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245 Cards in this Set
- Front
- Back
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What are acute complications of DM?
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-Hypoglycemia
-DKA -Hyperglycemia hyperosmolar non-ketotic coma (HHNC) |
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How is glucose derived in the body?
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Intestinal absorption
glycogenolysis gluconeogenesis |
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How do sulfonylurea oral hypoglycemics work?
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They stimulate the release of insulin from the pancreas
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What is the half-life of regular insulin in the circulation?
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3-10 minutes
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Name the 5 glucoregulatory hormones/
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insulin
glucagon epinephrine cortisol growth hormone |
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Which cells release insulin
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beta cells of the pancreatic islets
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Which cells release glucagon
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alpha cells of the pancreatic islets
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What are the 4 major types of diabetes?
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Type I diabetes mellitus
Type 2 diabetes mellitus Gestational diabetes IGT/IFG (impaired fasting glucose) |
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What reaction do urine ketone dipsticks use?
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nitroprusside
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what do urine ketones measure
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acetoacetate (not a good test for beta-hydroxybutyrate)
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Why are diabetic patients using insulin vulnerable to hypoglycaemia?
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insulin excess
failure of counter regulatory system |
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What is hypoglycaemia unawareness?
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-hypoglycemia without warning (decreased neurohormonal responses to episodes after even a single episode)
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What is the somogyi phenomenon?
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Increased insulin causing hypoglycaemia at night resulting in the AM rebound hyperglycaemia interpreted as inadequate insulin + propagated
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What test should be done if factitious hypoglycaemia is suspected?
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insulin antibodies or c-peptide (low to normal in exogenously given insulin)
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What is the treatment for hypoglycaemia?
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Adult: 25-75g of glucose IV (1-3 amps D50W)
Child: 0.5-1g/kg as D25W IV 2-4cc/kg Neonate: 0.2 g/kg as D10W - 1-2 mL/kg |
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What can you do to treat hypoglycaemia if IV access is not possible?
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1-2mg of glucagon IM (onset 10-20 min, peak 30-60min )
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When is glucagon ineffective for hypoglycaemia?
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when glycogen is absent (i.e.. alcohol-induced hypoglycaemia)
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What is the minimum acceptable observation period for patient period for patients with an OD of oral hypoglycaemic agents?
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24 hours and longer if hypoglycaemia is recurrent
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Which DM medications rarely cause hypoglycemia?
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Metformin
Thiazolidinedione |
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What agent can be added to the treatment regimen for patient with sulfonylurea OD? What is the dosage
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Octreotide (somatostatin analogue) 50-100ug IV or SQ q 12 hours
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What are the causes of hypoglycaemia in non-diabetic patients?
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Post prandial hypoglycemia
Fasting hypoglycemia |
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What is postprandial hypoglycaemia?
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Alimentary hyperinsulinism (see in patients with gastrectormy, gastrojejunostomy, pyloroplasty, vagotomy)
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What is fasting hypoglycaemia?
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Imbalance between glucose production and use
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What are the characteristics of HHNC?
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Hyperglycemia
Hyperosmolarity Dehydration decreased mental functioning (absence of ketosis or acidosis) |
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What is the pathophysiology of HHNC?
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-Decreased insulin, decreased peripheral uptake of glucose, hyperglycemia pulls fluid from intracellular to extracellular space.
-profound osmotic diuresis, limited by hypotension and decreased GFR -Therefore hyperglycaemia, hypernatremia, hypertonicity -circumstances often prevent patient from drinking sufficient fluids |
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On average what is the fluid deficit of an HHNC patient?
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9L
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Why are initial serum Na+ values inaccurate in HHNC?
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Hyperglycemia (use correction formula)
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What is the initial treatment for HHNC?
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2-3L NS (~1L/hr)
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What fluid should be used in HHNC following the initial resuscitation?
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1/2 NS
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When should dextrose be added?
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When glucose ~16mmol/L
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How is K+ repleted?
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Add 20-40mEq Kcl/L of fluid if renal function is adequate
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How is the fluid deficit corrected in HHNC?
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1/2 in the 1st 8 hours and the remainder over 24 hours
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Should phenytoin be used for seizures in HHNC?
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No, it is contraindicated as it may impair endogenous insulin release
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What are patients with HHNC at significant risk for?
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Thrombosis
Low dose SC heparin may be considered |
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Should insulin be used in the treatment of HHNC?
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Yes, but the glucose will correct rapidly with fluid (which is the most important therapy)
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What is the pathophysiology of increased ketones in DKA?
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-insulin deficiency activates enzymes that increase circulating FFA
-These FFA are oxidized and converted to acetoacetate and beta-hydroxybutyrate -also the body decreases the peripheral tissues use of ketones as fuel -increased production and decreased use |
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Are DKA patients always acidotic?
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No, patients may be alkalemic 2nd to protracted vomiting through alkalemia should prompt consideration of alcoholic ketoacidosis
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What % of DKA occurs in pts without previously diagnosed with diabetes?
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25%
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What are common complaints in DKA?
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Polydipsia
Polyuria Polyphagia Visual Blurring Weakness Weigh loss Nausea Vomiting Abdo pain |
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Is the glucose always elevated in DM?
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No, euglycemic (gluc <16) DKA has been reported in up to 18%
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Can VBGs be used to follow DKA?
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Yes!
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What tests should be ordered in DKA?
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VBG
cbc Ca++/Mg++/Po43/ ketone acetate lactate SMA-7 urinalysis |
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Why is the serum sodium value often misleading in DKA?
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Hyperglycemia
Hypertriglyceridemia Salt-poor fluid intake Increased losses |
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Why are Mg++, K+ and Po43- initially increased in DKA?
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Shifts from extracellular compartment
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What is the correction formula for K+ in acidosis
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subtract 0.6mEq/L from the lab K+ for every 0.1 decrease in pH
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which lab value should be used to predict the presence of infection in DKA?
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Increase in band neutrophils is 100% sensitive and 80% specific
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What is alcoholic ketoacidosis ?
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Similar to DKA (Kussmaul's, fruity odor to breath + acidemic ABG)
However they are euglycemic or hypoglycaemic the acidosis is caused by beta hydroxybutyric acid |
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What is the starting dose of insulin in DKA? Should a bolus be given?
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0.1U/kg/hr up to 5-10U/kg/hr. The bolus makes no significant difference in therapy
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How should insulin be given in DKA?
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IV - infusion. IM accomplishes the same effects but subjects the patient to repeated painful injections
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Which patients are more likely to develop cerebral edema? What is thought to precipitate it?
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Children
Rapid lowering of plasma osmolarity |
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Describe fluid replacement for DKA in children
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20cc/kg boluses of NS until SBP 80mmHg
then adjust rate to achieve urine output of 1-2cc/kg/hr (1/2 NS), add D5 when glucose <16mmol/L |
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Describe fluid admin in the 1st few hours of DKA in an adult
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1L over the 1st hour and in general, 2L over 1st 1-3hours
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When should K+ be added to solutions, how?
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-hypokalemic patients
-when the potassium is in the upper half of the normal range 20-40mEq/hr |
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What are the consequences of hypophosphatemia?
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-decreased 2,3 DPG, impaired O2 delivery to red blood cells
-decreased myocardial and respiratory muscle performance -hemolysis -impaired phagocytosis -thrombocytopenia -platelet dysfunction |
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What is the drawback to phosphorus administration?
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It has magnesium and calcium lowering properties
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How much magnesium is given in DKA?
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1-2g in 1st few litres if low
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When should bicarbonate be given in DKA? and how is it given?
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-severe acidemia (pH<7.0)
-44-88mEq/L (1-2 amps (50mEq/amp)) -pH should not be corrected above 7.1 |
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What are problems with bicarb administration in DKA
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-worsens inhibition of oxygen release to tissues
-rapid correction cases paradoxical csf acidosis -increased K+ requirement -potential for alkalosis -increased ketonuria -worse prognosis |
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What are iatrogenic causes of morbidity in DKA?
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-hypokalemia
-hypoglycemia -alkalosis -CHF -cerebral edema |
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When does cerebral edema occur?
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6-10 hours after initiation of therapy
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What factors are associated with cerebral edema in DKA?
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-low partial pressure of PaCo2
-increased initial BUN -show lack of increase in Na+ during therapy -bicarb admin (studied in children) |
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What is normal blood pH and why is it important that it be maintained within narrow limits?
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7.36-7.44
-protein and enzyme systems function properly only within a narrow pH |
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What is the difference between the term acidosis and academia?
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-Acidemia refers to an abnormal serum pH
-acidosis refers to processes that change the HCO3 or PaCO2 |
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What is the difference between the term metabolic and respiratory?
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Respiratory processes change the PaCO2 and Metabolic processes change the HCO3
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What is the difference between simple and mixed acid base disorder?
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Simple acid base disorders refer to a single acid-base disturbance with its compensatory response. Mixed disorders are the result of two or more primary disturbances
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What are 3 physiologic buffer systems and how do they work?
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1. Bicarbonate/Carbonic anhydrase buffer system. (Bicarbonate is present in large quantities and is important in the transient buffering of serum and interstitial fluid)
2. Intracellular Protein buffers: plasma proteins particularly albumin and hemoglobin can buffer large amounts of H+ 3.Bone as buffer: bone contains a large reservoir of bicarbonate and phosphate and can buffer a significant acid load |
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What are two compensatory mechanisms for acid-base disorders
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Pulmonary: respiratory drive is influenced by the effect of pH on chemoreceptors
Renal: more than 6-12 hours of sustained acidosis results in active excretion of H+ conversely more than 6 hours of alkalemia stimulates renal excretion of bicarbonate |
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How well do acid base compensatory mechanisms work?
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In general they return the pH toward normal over a period of 4-12 hours but do not fully normalize it.
Respiratory alkalosis is the only primary acid base disorder in which the pH does often normalize with time. |
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Describe the relationship between pH and potassium?
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In general, a change of 0.1pH unit causes an inverse change of approximately 0.6mEq
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Why would urine pH be low while serum pH is high?
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The kidney cannot compensate for alkalosis in the presence of hypokalemia. The kidney paradoxically excretes H+ in an attempt to retain K+.
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What does the anion gap provide an estimate of?
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Unmeasured anions in plasma mostly albumin, sulfate, phosphate and organic anions. When the AG is increased (>10) the clinician should consider an excess in organic acids or acidic substances
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Can a low anion gap be useful diagnostically?
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Low AG (<3) may be useful to diagnose
-lithium toxicity -immunoglobulin G myelomas -hypoalbuminemia of chronic disease |
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What is the delta gap?
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Delta gap =
(Calculated AG - 12) - (24- measured HC03) |
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How is the delta gap useful?
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Delta gap of >+6 = metabolic alkalosis or respiratory acidosis
Delta gap of <-6 = mixed disorder |
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Should you obtain blood gases only from arterial blood?
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The differences in blood gas parameters in acidemic patients are not clinically significantly different whether drawn from arterial, venous, capillary or intraosseous. In general venous access is preferred in adults and capillary in children
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What clinical features are seen in CO2 narcosis?
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HA
asterixis weakness tremors blurred vision confusion somnolence |
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What are broad categories of disorders that cause respiratory acidosis?
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-Airway obstruction
-Drugs that cause CNS depression -Hypoventilation -Pulmonary disease -thoracic cage disorders (PTX) -obesity with alveolar hypoventilation |
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What is the acute compensation for respiratory acidosis?
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HCO3 rises 1mmol/L for every 10mmHg elevation
this has minimal effect on the pH |
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What is the chronic compensation for respiratory acidosis?
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HCO3 rises 3.5mmol/L for every 10mmHg elevation
this nearly normalizes the pH |
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What are broad categories of disorders that can case respiratory alkalosis?
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Hypoxia mediated hyperventilation (high altitude, severe anemia, VQ mismatch)
CNS mediated (psychogenic, CVA, increased ICP) Pharmacologic (salicylate, epi, thyroxine) Pregnancy Septicemia Pulmonary Hepatic encephalopathy Hyponatremia |
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What clinical features are seen in respiratory alkalosis?
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Paresthesias of the lips and extremities
Lightheadedness Dizziness Muscle cramps Carpopedal spasms (symptoms are identical to those seen in hypocalcemia) |
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What is the acute compensation for respiratory alkalosis?
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HCO3 decreases by 2mmol/L for every 10 mmHg decrease in PaCO2
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What is the chronic compensation for respiratory alkalosis?
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HCO3 decreases by 5mmol/L for every 10mmHg decrease in pCO2 below 40mmHg
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What are the 3 main mechanisms for metabolic acidosis?
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Increased production of acids
Decreased renal excretion of acids Loss of alkali |
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List causes of Anion Gap Metabolic Acidosis?
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M - Methanol, malnutrition, metformin
U - uremia D - DKA P - Paraldehyde I - isoniazid, iron, inborn errors of metabolism L - lactic acidosis E - ethylene glycol C - Carbon monoxide, cyanide A - Alcoholic ketoacidosis, alcohol intoxication T - toluene S - Salicylates |
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What are the causes of normal anion gap metabolic acidosis?
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H - Hyperalimentation, Hyperparathyroidism, Hypoaldosteronism, Hyperkalemia
A - acetazolamide R - RTA D - Diarrhea U - Ureteroenteric fistula P - Pancreaticoduodenal fistula |
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What is the most common cause of non-anion gap metabolic acidosis?
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Diarrhea
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How can you differentiate normal anion gap metabolic acidosis from GI loss vs altered urinary acidification?
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Calculate the urinary anion gap
UAG = (Na+ + K+) - Cl- Negative UAG suggests GI losses, positive UAG suggests renal tubule abnormality |
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What is the acute compensation for metabolic acidosis?
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Respiratory center is stimulated to increase alveolar ventilation and decrease PaCo2 (max response after 12-24 hours)
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How do you manage patients with metabolic acidosis?
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Treat the underlying cause
Look for and treat severe hyperkalemia Consider NaHCO3 1mmol/kg for pH <7.1 unless the condition is self-limited. |
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What are complications of treating metabolic acidosis with NaHCO3?
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Hypokalemia
Hypocalcemia Hypernatremia Hyperosmolality Volume overload Overshoot alkalosis Impaired oxygen delivery Paradoxical CNS intracellular acidosis |
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Explain paradoxical CNS acidosis caused by giving sodium bicarb)
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Bicarbonate penetrates the BBB very slowly.
IV bicarb alkalinizes the plasma much faster, which activates the peripheral chemoreceptors which decreases MV and causes PaCO2 to rise. The PaCO2 crosses the BBB quickly. |
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What causes metabolic alkalosis?
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There needs to be an initiating process and another process that maintains the disorder (kidneys have a huge capacity to excrete bicarbonate)
Initiating: -gain of alkali in the ECF (bicarb infusion, citrate, milk alkali, hepatic metabolism of organic acid ions) -loss of hydrogen ions (diuretics, vomiting) Maintaining processes -chloride deficiency (most common) vomiting, loop and thiazide diuretics, post hypercapnia, villous adenoma, chloride diarrhea) -mineralocorticoid excess (hyperaldosteronism, cushings, diuretics, licorice, bartters) -reduced GFR -ECF volume depletion Loss of gastric acid and diuretic use account for 90% of the clinical cases of metabolic alkalosis |
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What are adverse effects of alkalosis?
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Decreased myocardial contractility
Arrhythmias Decreased CBF Confusion Mental obtundation Neuromuscular excitability Impaired peripheral oxygen unloading |
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Outline your management of metabolic alkalosis?
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Correct cause (correct pyloric obstruction, cease diuretics, give PPI to decrease gastric acid losses)
Correct the deficiency which is impairing renal bicarb excretion (Cl, water and K+) Expand ECF volume with NS Rarely need ancillary measures (HCl, acetazolamide, oral lysine hydrochloride) Supportive measures Avoid hyperventilation as this worsens alkalemia |
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What is the formula for respiratory compensation in metabolic acidosis?
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PaCo2 = 1.5(HCO3) + 8
(range +/-2) (the last 2 digits of the pH should = PaCO2) Limit of compensation is 10mmHg |
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What is the formula for respiratory compensation in metabolic alkalosis?
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PaCO2 = 0.7(HCO3) + 21
(range +/-5) (PacO2 increases 0.6 for every 1 increase in HCO3 to max of 55) |
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What is the effect of hypoalbuminemia on AG?
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For every 10 drop in albumin, AG decreases by 2.5
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What blood work should you order in AG metabolic acidosis?
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KULTS
ketones Urea Lactate Toxic alcohols Salicylates |
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How do you calculate an osmolar gap?
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OG = Measured - Calculated
calculated = 2x Na+ BUN + glucose + 1.5(alcohol) |
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What is the differential for an osmolar gap?
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AID MEE
Acetone (DKA, AKA) Isopropyl alcohol Diuretics (mannitol, sorbitol, glycerol) Methanol Ethylene Glycol Ethyl ether |
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How is water compartmentalized in the human body?
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Intracellular space (2/3)
Extracellular space (1/3) (interstitial and intravascular) |
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Describe the function of antidiuretic hormone?
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It enhances water re-absorption by the kidneys
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What factors cause the release of ADH?
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-increased serum osmolality or decreased intravascular volume or BP
-release stimulated by angiotensin, catecholamines, opiates, caffeine, hypoglycaemia, hypoxia, stress |
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what are the major types of hyponatremia?
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Hypovolemic (TBW decreases, total body sodium decreases more)
Euvolemic (TBW increases, total sodium remains the same) Hypervolemic (Total body sodium increases and total body water increases more) Redistributive (water shifts from intracellular to the extracellular compartment) Pseudohyponatremia (diluted by excessive proteins and lipids, total body sodium is unchanged) |
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What are examples of hypovolemic hyponatremia?
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Renal losses
Gi losses Third spacing Sweating Addisons |
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What are examples of euvolemic hyponatremia?
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SIADH
Psychogenic polydipsia Administration of hypotonic fluids Hypoadrenalism Hypothyroidism |
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What are examples of hypervolemic hyponatremia?
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CHF
Cirrhosis Nephrotic syndrome Renal failure |
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What are examples of re-distributive hyponatremia?
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Hyperglycemia
Mannitol |
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What are examples of pseudohyponatremia?
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Hypertriglyceridemia
Multiple myeloma |
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How can you correct for redistributive hyponatremia?
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For every 4mmol/L elevation in glucose expect a fall of 1mmol/L in sodium
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what is the hallmark of SIADH?
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An inappropriately concentrated urine despite the presence of a low serum osmolality and a normal circulating blood volume.
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What are causes of SIADH?
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CNS disease (tumor, trauma, infection, CVA, SAH, GBS, MS)
Pulmonary disease (tumor, pneumonia, COPD, lung abscess, TB, CF) Carcinoma (lung, pancreas, thymoma, ovary) Drugs (carbamazepine, haldol etc.) Surgery (post-op) Stress |
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What are the clinical features of hyponatremia and at what level of sodium do they become manifest?
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Lethargy
Apathy Confusion Disorientation Agitation Depression Focal neuro deficits Ataxia Seizures Symptoms are more pronounced if the drop in sodium is sudden. Usually a level below 120mmol/L will result in symptoms |
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How does urinary sodium help to determine the etiology of hyponatremia?
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U Na <20mmol/L non renal cause
U Na >20mmol/L renal cause |
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How does MDMA cause hyponatremia?
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Increased water intake, excessive sweating with physical exertion and the release of vasopressin
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What test can help you differentiate between true hyponatremia and pseudohyponatremia?
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Serum osmolarity
It is abnormally low in patients with hyposmolar hyponatremia but it is normal in patients with pseudohyponatremia |
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How should you treat patients with chronic/non-severe hyponatremia?
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Hypovolemic hyponatremia -> correct volume deficits with isotonic saline
Euvolemic hyponatremia-> restrict free water intake and let internal medicine figure it out Hypervolemic hyponatremia: restrict free water intake, consider diuresis although this will increase sodium excretion |
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What are signs of severely symptomatic hyponatremia?
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Seizures
Focal findings Coma |
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What is the treatment for severely symptomatic hyponatremia?
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100cc 3% saline over 10 minutes
then give 100cc 3% saline over 50 minutes then STOP (this will increase the serum sodium by 3-6mEq) |
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At what rate is it safe to correct hyponatremia? What is the danger of correcting too quickly?
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No faster than 0.5mmol/hour or 10-12 mmol/day
The risk is central pontine myelinolysis (flaccid paralysis, coma, death 1-2 days post correction) |
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What are the main causes of hypernatremia?
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-Lack of free water
-Diabetes insipidus (central or nephrogenic) |
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What is diabetes insipidus?
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A condition in which the kidneys fail to concentrate the urine because of decreased ADH secretion or decreased action of ADH in the kidneys
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what are causes of diabetes insipidus?
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Central
Idiopathic Head trauma CNS tumor, hemorrhage, infection, granulomatous disease Nephrogenic DI Chronic renal insufficiency Lithium toxicity Hypercalcemia Hypokalemia Tubulointerstitial disease |
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What intravenous fluid should be used in hypernatremic patients who are volume depleted and show signs of organ hypo perfusion?
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Isotonic saline should be given until the patient is hemodynamically stable
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How do you calculate the hypernatremic patient's free water deficit?
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(0.6x body weight) x {(Na/140)-1}
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How quickly should you correct hypernatremia?
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0.5mmol/L per hour or 10-12 mmol/L per day
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What is the danger of correcting hypernatremia too quickly?
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Cerebral edema
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How much potassium is in the average adult human body and where is it found?
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2500-3000mmol of K+
98% is found in the intracellular compartment. |
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What are major causes of hypokalemia?
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Decreased intake
-malnurtition Increased losses -diuretics -Gi losses -hypomagnesemia -hyperaldosteronism (Primary: Conn's syndrome, adrenal hyperplasia or Secondary: CHF, cirrhosis, nephrotic syndrome, dehydration) -Adrenocorticoid excess (cushing's, steroids) -RTA Transcellular shifting -alkalosis -insulin -beta agonists -hypokalemic periodic paralysis |
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Why does vomiting cause hypokalemia?
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Vomiting itself does not cause K+ loss rather hypokalemia results from hypovolemia, secondary hyperaldosteronism and alkalosis
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What are the clinical features of hypokalemia?
|
Neuromuscular
-lethargy, depression, irritability, confusion -paresthesias, depressed DTR, fasciculations, myalgias, prominent muscle weakness CV -palpitations, postural hypotension, ectopy and dysrhythmias GI -nausea, vomiting, abdominal distension, paralytic ileus Renal -polyuria, polydipsia, impaired ability to concentrate urine Acid base balance: metabolic alkalosis Rhabdomyolysis |
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How can you estimate the total potassium deficit from the serum level.
|
Once the level is 3.5mmol/L the deficit is about 100mmol. For every 0.3mmol/L below 3.5 there is a deficit of 100 mmol more.
It is also important to consider that a large portion of the administered K is excreted by the kidneys, even in the face of total body depletion |
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What is the best way to replace potassium in the depleted patient?
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Oral therapy is preferred, the amount given intravenously is limited by the risk of causing dysrhythmia and the pain associated with infusion
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How much potassium can safely be given IV?
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Not more than 20mmol/hour at concentrations of 40mmol/L (at concentrations of >20mmol/L the patient should be on a cardiac monitor)
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How can K+ be given through a peripheral IV?
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10mmol in 100cc fluid over 20-30 minutes and repeated as necessary
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What coexisting condition should you think of when the serum potassium doesn't correct despite replacement?
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Magnesium depletion reduces the intracellular potassium concentration.
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What are the main causes of hyperkalemia in ED patients?
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-Spurious (hemolysis of sample, extreme thrombocytosis or leukocytosis)
-Increased intake (supplements, stored blood) -Impaired excretion (renal failure, K+ sparing diuretics, hypoaldosteronism) -Transcellular shifts (acidosis, beta blockers, digitalis toxicity, succinylcholine) -cell death (rhabdo, invivo hemolysis, tumor lysis, burns, crush) |
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What are the clinical features of hyperkalemia?
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ECG: peaked T waves, prolonged PR, loss of P, widening of the QRS, sine wave
Dysrhythmias: second and third degree heart block, wide complex tachycardia, ventricular fibrillation and asystole Neuromuscular: muscle cramps, weakness, paralysis, paresthesia, tetany, focal neuro deficits |
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How do you treat hyperkalemia?
|
-Patient should be on a cardiac monitor
-calcium chloride only for a wide QRS. 10cc of 10% solution over 10 minutes. -insulin 10U plus glucose 50grams (drops level by 1mEq) -beta agonists (drops by 0.5mEq) -NS: only if dehydrated or going for dialysis -bicarbonate 1-2 amps slow IV push (only if acidotic) -forced diuresis -ion exchange resin (30-60gm kayexalate oral or rectal) -dialysis |
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How much calcium is in the body?
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1200grams
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Where is calcium in the body?
|
99% in the bone
Remaining 1% is -bound to serum proteins -free ionized calcium (physiologically active) -complexed with serum anions |
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What happens when serum calcium levels fall?
|
-PTH stimulates increased bone turnover and release of calcium into the serum
-PTH stimulates increased resorption of Ca in the distal tubule -PTH activates vitamin D which increases absorption of CA in the gut -Rising serum Ca suppresses PTH and releases calcitonin which decreases osteoclastic activity and enhances skeletal deposition of calcium |
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What are the effects of pH on serum calcium?
|
Acidosis decreases calcium binding to albumin
Alkalosis increases calcium binding to albumin In both cases the ratio of bound to ionized calcium is changed without altering the total measured calcium |
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What are the main causes of hypocalcemia?
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Hypoparathyroidism
-Primary (rare) -Secondary (neck surgery, metastatic carcinoma, infiltrative disorders, sepsis, pancreatitis, burns, hypomagnesemia, hypermagnesemia) Vitamin D insufficiency (malnutrition, malabsorption, renal failure) PTH resistance (pseudohypoparathyroidism - rare) Calcium chelation (hyperphosphatermia, citrate, alkalosis, fluoride poisoning, fre fatty acids) |
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What are the clinical features of hypocalcemia?
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Neuromuscular: paresthesias, weakness, muscle spasms, tetany, Chvostek and Trousseau's signs, hyperreflexia, seizures
Cardiovascular: bradycardia, hypotension, CHF, QT prolongation, cardiac arrest Pulmonary: bronchospasm and laryngeal spasm Psychiatric: anxiety, irritability, congusion, psychosis |
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What is Chvostek's sign?
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Tapping over the facial nerve causes twitching of the ipsilateral facial muscles
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What is Trousseau's sign?
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Carpal spasm in response to inflation of an arm blood pressure cuff to 20mmHg above SBP
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Outline your treatment of hypocalcemia
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-If patient is asymptomatic, check the ionized calcium level
-If the patient is symptomatic, treat without verifying the ionized calcium level -Put the patient on a cardiac monitor -Given an amp of calcium chloride or gluconate -This lasts 1-2 hours so repeat the dose -symptoms that are refractory to appropriate doses of calcium may be caused by co-existing hypomagnesemia. In patients with normal renal fuction, administer 2-4 g of 10% magnesium sulfate -patients with asymptomatic hypocalcemia can be treated with oral calcium supplements |
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What are side effects of IV calcium administration?
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Hypertension
Nausea Vomiting Flushing Bradycardia and heart block occur in rare cases It can also cause severe tissue necrosis if extravasation occurs therefore whenever possible calcium chloride should be diluted in 5% dextrose in water |
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What are the main causes of hypercalcemia?
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PAM P SCHMIDT
P - hyperparathyroidism A - Addison's disease M - Multiple myeloma P - Paget's disease S - sarcoidosis C - cancer M -milk alkali syndrome I - immobilization D - excess vitamin D T - thiazides |
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What are the clinical features of hypercalcemia?
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bones, stones, groans with psychiatric overtones (though this does not include the CV side effects)
GI - nausea, vomiting, pancreatitis, constipation CV - hypertension, bradycardia, shortened QT, prolonged PR, widened QRS, ventricular dysrhythmias CNS - fatigue, weakness, confusion, depression, apathy, psychosis GU - stones, renal failure, polyuria Muscular: bone pain, fractures, weakness |
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What is your management of hypercalcemia?
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-Saline diuresis (2-5L/day)
-furosemide 10-40mg IV q6-8 -osteoclast inhibitors (calcitonin, bisphosphonates, glucocorticoids) -address underlying cause |
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What are the main causes of hypomagnesemia in ED patients?
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Alcohol abuse
Diuretic use Renal losses (renal failure, renal transplantation) GI losses (hyperemesis, diarrhea, NG suction, short bowel) Endocrine disorders (DM, hyperaldosteronism, hyperthyroidism, hyperparathyroidism) Pregnancy |
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What are the clinical features of hypomagnesemia?
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Neuromuscular: muscle weakness, tremor, hyperreflexia, tetany and a positive Chvostek's or Trousseau's sign
CV: SVT(afib, MAT, PSVT), ventricular dysrhythmias (PVC, vtach, torsades, vfib) |
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When should magnesium be given in the ED?
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-Patients with low serum levels
-Patients with normal serum levels but associated conditions that would suggest magnesium deficiency -Patients with refractory hypokalemia or unexplained hypocalcemia -Can also be used to treat certain conditions: asthma, torsades, eclampsia |
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What are possible AE of parenteral magnesium replacement?
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-Venous irritation
-bradycardia -hypotension -weakness, depressed DTR -depressed LOC -respiratory depression -severe, symptomatic hypomagnesemia with seizures or other severe symptoms (2-4g MgSo4 over 5-10 minutes) -in less severe cases give smaller IV doses over several days or replace with oral salts (limited by diarrhea) |
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What are the major causes of hypermagnesmia in ED patients?
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Renal failure in conjunction withe an exogenous or endogenous magnesium load (antacids, laxatives, IV magnesium, rhabdo, tumour lysis)
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What are the clinical manifestation of hypermagnesemia?
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-Nausea, vomiting, weakness, cutaneous flushing
-hyporeflexia -Hypotension |
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What are the ECG findings of hypermagnesemia?
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-QRS widening
-QT and PR prolongations -conduction abnormalities -respiratory depression, coma, complete heart block -asystole, cardiac arrest, death |
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What is the management of hypermagnesemia?
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DC exogenous magnesium
IV isotonic fluids and furosemide to accelerate elimination If severe: IV calcium Consider dialysis in patients with coma, respiratory failure or hemodynamic instability |
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Where is phosphorus in the body?
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-in cells as a component of RNA and DNA and of the phospholipid cell membrane
-in bone -in serum as an acid-base buffer |
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What are the major causes of hypophosphatemia?
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-Renal losses (diuretics, DKA, hyperparathyroidism)
-Insufficient intestinal absorption (malnutrition, alcoholism, chronic diarrhea) -Transcellular shifts (alkalosis, glucose containing solutions) |
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What are the clinical manifestations of hypophosphatemia?
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CV: myocardial depression, hypotension, ventricular dysrhythmias
Pulmonary: respiratory failure (muscle weakness) Skeletal muscle weakness Hematoloic: decreased tissue oxygen delivery, hemolysis, leucocyte and platelet dysfunction Neurologic: paresthesias, seizures coma |
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What is your management of hypophosphatemia?
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Mild to moderate: oral supplements
Severe: IV potassium phosphate or sodium phosphate |
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What are complications of IV phosphate administration?
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Acute hypocalcemia
Hyperphosphatemia Calcium phosphate deposition in tissues |
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What are the major causes of hyperphosphatermia?
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Spurious (paraproteinemia, hyperlipidemia, hemolysis, hyperbilirubinemia)
Renal (renal failure, hypoparathyroidism, thyrotoxicosis, vitamin D excess) Cellular injury (rhabdo, TLS) Increased intalke (laxatives, enemas, IV or oral supplements) |
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What are the clinical manifestations of hyperhphosphatermia?
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Reflect the associated hypocalcemia that results when excess serum phosphate binds with calcium and precipitates in the tissues
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What is your management of hyperphosphatemia?
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Treat hypocalcemia
Isotonic saline to increase clearance in patients with normal renal fuciton Insulin/dextrose in life threatening cases HD or PD should be considered |
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What is myoglobin?
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The major heme protein supplying oxygen to skeletal and cardiac muscle. It has a higher affinity than hemoglobin for oxygen so facilitates influx of oxygen into muscle cells
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What is the pathophysiology of rhabdomyolysis renal failure?
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Plasma myoglobin is normally bound to haptoglobin but with muscle damage this is overwhelmed and free myoglobin is filtered by the glomerulus and when coupled with hypovolemia precipitates in the tubules causing ARF
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How commonly does AKI develop in patients with rhabdomyolysis?
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30-40% of patients
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What are predictors of AKI in rhabdomyolysis?
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CK>6000
Dehydration Sepsis Hyperkalemia or hyperphosphatemia hypoalbuminemia |
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What are non-traumatic causes of rhabdo?
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Immobilization
Exercise Alcohol Drugs/toxins (cocaine, MDMA, PCP, statins, CO, snake bites) Infections Seizures Electrolyte abnormalities (hypophosphatemia and hypokalemia) Electrical injuries Hyperthermia/hypothermia Metabolic myopathies |
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What are the most common viral, bacterial and parasitic causes of rhabdo?
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Influenza A and B
Legionella Falciparum malaria |
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What are clinical features of rhabdo?
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muscle weakness, myalgias, tea colored urine
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What is the limitation of myoglobin as a test for rhabdo?
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Half life is 1-3 hours and can be cleared completely within 6 hours
Urine myoglobin is also cleared quickly |
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What are the kinetics of creatine kinase in rhabdo?
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Half life 1.5days
peaks within 24-36 hours levels decrease by 39% per day, failure to do so suggests ongoing muscle injury (?compartment) |
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What level of CK defines rhabdo?
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It is not defined by a specific CK level
In general in the absence of cerebral or myocardial infarction a CK above 5000 indicates serious muscle injury In the presence of dehydration ARF has been seen with CK levels as low as 2000 |
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What laboratory findings are typically seen in rhabdomyolysis?
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Hyperkalemia
Hyperphosphatemia Hypocalcemia Hypercalcemia Hyperuricemia Hypoalbuminemia DIC Elevated AST, ALT and LDH |
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List causes of pigmenturia other than rhabdo?
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Hemoglobinuria
Hematuria Acute intermittent porphyria Bilirubinemia Drugs: vitamin B12, rifampin, phenytoin, laxatives |
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What are the goals of management in rhabdomyolysis?
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Treat underlying cause
Manage electrolyte derangements Prevent renal failure Prevent coagulopathy Early detection and management of compartment syndrome |
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What is your treatment of rhabdomyolysis?
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-Saline infusion titrated for urine output of 200-300cc/hr (may require up to 20L in the first 24 hours) avoid potassium containing fluids
-mannitol (controversial due to lack of high quality evidence) -avoid loop diuretics as they can acidify the urine -urine alkalinization - has theoretical advantages mainly that precipitation of myoglobin is increased in acidic urine but studies have been unconvincing. There is some evidence that it may be beneficial when CK >30,000U/L. If you choose to used it put 2 ampules in 1LD5W aiming for a urine pH >6.5. Monitor urine pH, bicarb, calcium and potassium levels -treat hyperkalemia -avoid correcting hypocalcemia if asymptomatic -symptomatic hypercalcemia generally only requires volume expansion and diuretics therapy -dialysis may be necessary -monitor and treat for compartment syndrome -search for an correct underlying cause |
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Describe the normal physiology of thyroid hormone
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-Hypothalamus produces thyrotropin releasing hormone (TRH)
-TRH stimulates anterior pituitary to secrete TSH -TSH triggers release of thyroid hormone by the thyroid gland -The thyroid gland produces prohormone thyroxine (T4) which is deiodinated to its active form (T3), the thyroid also produces a small amount of T3 -Thyroid hormone is regulated by negative feedback by circulating thyroid hormones on the pituitary -T3 and T4 exist in free unbound portion (biologically active) and a portion that is protein bound -unbound T3 is the biologically active hormone |
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What is reverse T3
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-During systemic illness, deiodination occurs but at an inner ring of T4 instead of an outer rink and produces reverse T3
-Reverse T3 is inactive |
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What is the effect of iodide on thyroid hormone production?
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-iodide is a substrate for thyroid hormone production
-excess iodide transiently inhibits iodide trapping and blocks the release of thyroid hormone -an iodide load can induce hyperthyroidism in patients with multinodular goiter and latent fraves disease especially in those that are iodine deficient |
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What is the effect of T3 and T4 on beta adrenergic receptors?
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T3 and T4 increase the number and sensitivity of beta adrenergic receptors and dramatically increase the response to endogenous catecholamines
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What is the difference between hyperthyroidism and thyrotoxicosis?
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Hyperthyroidism refers to inappropriately elevated thyroid function
Thyrotoxicosis refers to an excessive amount of circulating thyroid hormone |
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What is Graves' disease?
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-Autoimmune disorder in which B lymphocytes produce immunoglobulins that stimulate the TSH receptor
-Most common cause of thyrotoxicosis -Primarily affects women between 20 and 40 |
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What is a toxic multinodular goitre?
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-Spectrum of disease ranging from a single hyper functioning nodule within a multi nodular thyroid to a gland with multiple areas of hyperfunction
-milder more gradual onset compared to Graves |
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What is thyroiditis?
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Thyroid gland inflammation and cell breakdown with release of preformed thyroid hormone
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List and describe causes of thyroiditis
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Autoimmune
Hashimoto, postpartum, sporadic Infectious Dequervains, suppurative Drugs Amiodarone, interferon, interleukin-2, GCSD and lithium |
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What is thyrotoxicosis factitia?
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-chronic excess ingestion of thyroid hormone resulting in thyrotoxicosis
-usually medical personnel with psychiatric disease -usually only manifest minor toxicity because of 7day half life of T4, the suppression of T4 to T3 conversion and inhibition of endogenous hormone |
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What are the patients complaints in thyrotoxicosis
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Constitutional Weight loss despite hyperphagia, fatigue, generalized weakness
Hypermetabolic: heat intolerance, cold preference, excessive perspiration Cardiorespiratory: heart pounding and racing, dyspnea on exertion, chest pain Psychiatric: anxiety, restlessness, hyperkinesis, emotional lability, confusion Muscular: tremor Ophthalmologic: tearing, irritation, diplopia Thyroid: neck fullness Dem: pretibial swelling, flushed feeling Repro: oligomenorrhea, decreased libido |
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What are the physical exam findings in thyrotoxicosis?
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VS - tachycardia, wide pulse pressure, bounding pulses, fever
Cardiac: hyperdynamic precordium, systolic flow murmur, prominent heart sounds, systolic rub, tricuspid regurg, afib, heart failure Ophthalmologic: widened palpebral fissures, lid lag, globe lag, proptosis Neuro: fine tremor, hyperreflexia, proximal muscle weakness Psychiatric: emotionally labile, poor concentration Derm: warm, moist skin, fine, brittle hair neck: diffuse symmetrical thyroid enlargement, sometimes with a bruit and palpable thrill |
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What is myxedema?
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Accumulation of hyaluronic acid in the dermis producing a mucinous edema that is responsible for the thickening of features and puffy appearance seen with full blown hypothyroidism
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What is lid lag?
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Upper lid lags behind the globe when the patients is asked to look down slowly
Seen in Graves ophthalmopathy |
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What is globe lag?
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Globe lags behind the upper lid with slow upper gaze
Seen in Graves ophthalmopathy |
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What is thyroid storm?
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-life-threatening decompensation of poorly controlled, untreated or unrecognized thyrotoxicosis seen predominantly in Graves
-exaggeration of the clinical manifestations of thyrotoxicosis plus fever, tachycardia, CNS dysfunction and GI symptoms. -decompensation of one or more organ systems such as shock or heart failure also defines thyroid storm -It is uniformly fatal if untreated |
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What is the pathophysiology of thyroid storm?
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Increase in catecholamine binding sites leads to heightened response to adrenergic stimuli
Superimposed acute stress results in outpouring of catecholamines that in conjunction with high levels of free T4 and T3 precipitates the exaggerated response |
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What are common precipitants of thyroid storm?
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infection
MI CVA PE DKA Parturition Trauma Contrast media Amio Surgery |
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What are the clinical manifestations of thyroid storm?
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Fever out of proportion (>41C)
Excessive diaphoresis Sinus tachycardia Rapid afib or SVT CHF AMS Nausea, vomiting, diarrhea Cholestatic jaundice |
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How can you distinguish between thyrotoxicosis and thyroid storm?
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Burch and Wartofski developed a scoring system to help distinguish.
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what is the best screening test for thyrotoxicosis?
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TSH - a normal result excludes hyperthyroidism
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what lab abnormalities (other than TSH) are seen in thyrotoxicosis?
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Hyperglycemia
Mild Hypercalcemia Mild increase is AST, ALT, LDH, ALP, bilirubin Leukocytosis with left shift mild normocytic normochromic anemia low serum cholesterol |
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What lab test can differentiate between fictious thyrotoxicosis and true thyrotoxicosis?
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Thyroglobulin levels are very low in factitious thyrotoxicosis but elevated in all other forms
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What is the differential diagnosis of thyrotoxicosis
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Psychiatric
-mania -anxiety Drug intoxication -sympathomimetic -anticholinergic -withdrawal Other causes of high fever -heat stroke -NMS -SS -Bacterial meningitis -Sepsis |
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Which patient groups are more likely to present with apathetic thyrotoxicosis and what are its features?
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Elderly with multinodular goitre
Masked hyperadrenergic features, facial muscles lack expression, mental status depressed New onset afib with CHF is often the presenting symptoms |
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What medical intervention must be avoided in patients with thyrotoxicosis
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Iodine load (amiodarone, iodinated contrast media)
Drugs that may interfere with protein binding leading to increased free T3 and T4 - salicylate, NSAIDs Drugs that increase sympathetic tone - pseudo ephedrine, ketamine, albuterol |
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What are the goals in the treatment of thyroid storm?
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Reduce thyroid hormone production
inhibit thyroid hormone release block peripheral conversion of T4 to T3 initiate beta adrenergic blockade supportive measures identify and treat the precipitating event |
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What is your management plan for thyroid storm
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Propylthiouracil 600-1000mg PO or PR loading dose then 200-250mg q 4hours
(alternative methimazole 20-25 mg PO or PR initially then 20-25mg q 4 hours) (this reduces thyroid hormone synthesis) Saturated solution of potassium iodide (SSKI) 5 drops by mouth every 6 hours Lugols solution Sodium iodide 500mg solution q12hour or lithium carbonate 300mg by mouth or NG q 6hours (this inhibits the release of thyroid hormone) Block beta receptors -Propranolol 60-80mg q 6hours -metoprolol 50mg PO q12hours Propranolol 0.5-1.0mg IV slow push test dose then repeat every 15 minutes until desired effect, then 2-3 mg q 3hours Esmolol 250-500mcg bolus then 50-100 mcg/kg/min If strict contraindication to betablocker then reserpine 0.5mg PO q 6hours (block beta receptors) Hydrocortisone 300mg IV followed by 100mg IV q 6hours or dexamethasone 2-4mg IV q 6hours (blocks the peripheral conversion of T4 to T3) Supportive measures -volume resuscitation -D5 or NS 125-1000mL/hour depending on volume status and CHF -Acetaminophen with caution (?hepatic dysfunction) -Cooling blankets, fans, ice packs, ice lavage Lorazepam or diazepam as anxiolytic L-carnitine (blocks the entry of thyroid hormone into cels) cholestyramine (blocks the enterohepatic circulation of thyroid hormone |
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How should you time the administration of iodine in your treatment of thyroid storm and why?
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Administration should be delayed at least 1 hour after PTU or methimazole because an iodine load presented to an actively synthesizing gland provides further substrate
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Under what circumstances should iodine not be used in the treatment of thyroid storm?
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Iodine allergy
thyroid storm induced by amiodarone or iodinated contrast media (use lithium under these circumstances) |
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Which beta blocker is preferred in the treatment of thyroid storm and why?
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Propranolol because it blocks conversion of T4 to T3 and its nonselective effects also improve tremor hyperpyrexia and restlessness
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How does the management of atrial fibrillation in thyrotoxicosis differ from other cases?
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-higher doses of beta blocker is usually needed
-calcium channel blockers should be avoided as hypotension is a potential complication -digoxin tends to be ineffective -amiodarone is contraindicated -attempts at cardioversion are usually fruitless and should be postpones until the patient is euthyroid |
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How does your management of thyrotoxicosis differ when it is caused by subacute thyroiditis or exogenous thyroid hormone ingestion?
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-There is no role for thionamides and iodine
-Mainstay is beta blockade |
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What is the most serious complication of PTU and how does it initially present?
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Agranulocytosis (heralded by sore throat)
Infrequently hepatitis, vasculitis and polyarthritis |
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What is the definition of subclinical hypothyroidism?
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TSH elevation with normal free T4
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What are the main causes of hypothyroidism?
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Worldwide: iodine deficiency
US: autoimmune thyroid disease |
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What are the causes of hypothyroidism?
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Primary
-autoimmune (Hashimoto's) -Post partum thyroiditis -Subacute thyroiditis -Drugs - amiodarone, interfereon alpha, thalidomide, lithium -iatrogenic (radioacive iodine treatment of Graves) -iodine deficiency Central -pituitary adenoma -tumors impinging on the hypothalamus -history of brain irradiation -Drugs (dopamine, lithium) -Sheehan syndrome -Genetic disorder |
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What are the clinical manifestations of hypothyroidism?
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VS - SBP normal or low, DBP normal or elevated, slow pulse, slow shallow respirations, prone to hypothermia
Hypometabolic complaints - cold intolerance, fatigue, weight gain but decreased appetite Cutaneous - coarse, brittle hair, alopecia, dry, coarse skin, decreased perspiration Neurologic - neurocognitive impairment, agitation, psychosis, seizures, ataxia, dysmetria Muscular - proximal myopathy Cardiac - long QT, diastolic heart failure, pericardial effusion, peripheral edema GI - constipation Reproductive - oligo and amenorrhea/menorrhagia Rheumatic - polyarthralgias HEENT - hoarseness, macroglossia, periorbital swelling |
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What is the best way to elicit hung up reflexes in the hypothyroid patients? What other conditions are associated with this finding?
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-Achilles tendon reflex performed while patient is kneeling
Also seen with aging, diabetes, pregnancy |
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What is myxedema coma?
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-Life threatening decompensation of severe long standing hypothyroidism
-Hallmarks of myxedema coma are altered mental status, hypothermia, hypotension, bradycardia, hypoventilation are often present -Progressive weakness, lethargy, immobility may progress to shock and death |
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What are the most common precipitants of myxedema coma?
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infection
cold exposure trauma CVA CHF GI bleeding Drug effects: sedatives, narcotics, general anesthesia, thyroid hormone non compliance, amiodarone, lithium, iodide, phenytoin, rifampin |
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Which thyroid functions test should be used to confirm the diagnosis of hypothyroidism?
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-TSH alone is a good screening test
-Free T4 should be added if TSH is abnormal -Total T4 is not useful because of confounding factors on protein binding -T3 is not reliable because almost any physiologic stress can lead to decreased peripheral conversion of T4 to T3 |
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What should hypoglycemia make you consider in the patient with myxedema coma?
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May be a clue of concomitant adrenal insufficiency which is present in 10% of myxedema coma patients
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Which patients newly diagnosed hypothyroidism should be started on a smaller dose than usual of levothyroxine?
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Elders and patients with underlying CAD
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How frequently should levothyroxine doses be adjusted?
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It has a long half life and gradual conversion to T3 so small adjustments should be made no more often than every 6 weeks
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What is special about managing the airway in patients with myxedema coma?
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-Partial obstruction from macroglossia and supraglottic edema
-respiratory muscles may be weak causing central hypoventilation and CO2 retention, life threatening alkalosis can occur during the initial phase of full ventilator support |
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How should you fluid resuscitate a patient with myxedema coma?
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Carefully - volume depletion is prominent but aggressive replacement risks unmasking congestive heart failure
-use D5NS because patient is at high risk for hyponatremia and hypoglycemia |
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When should thyroid hormone replacement begin in the patient with suspected myxedema coma?
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If myxedema coma is suspected clinically, start right away without waiting for confirmatory tests
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How should thyroid hormone be replaced in myxedema coma?
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-T4 has lower risk of toxicity (it must be converted to T3) so it is preferred for elders and those with cardiac co-morbidity
-T3 has quicker onset of action and increased biologic activity so it is preferred in the critically ill younger patients without cardiac co-morbidity where rapid correction is desired -Due to impaired oral absorption and transit of medications in myxedema coma, the IV route is recommended until the patient is alert and able to tolerate oral medications |
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What other treatments should be administered to patients with myxedema coma?
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Hydrocortisone should be administered to all patients because many will have either central hypothyroidism with ACTH deficiency, autoimmune destruction of the thyroid and adrenal glands or relative adrenal insufficiency unmasked by stress.
Hydrocortisone is given 50-100mg IV q 6-8 Hypothermia is treated with passive rewarming using regular blankets and prevention of further heat loss. Heated blankets could be employed but there is a risk that resulting vasodilation will lead to a fall in peripheral vascular resistance and hypotension If hyponatremia is profound and associated with serious symptoms treat with hypertonic saline |
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What is the main difference between primary and secondary adrenal insufficiency?
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In primary adrenocortical insufficiency glucocorticoid and mineralocorticoid properties are lost
Secondary adrenocortical insufficiency (secondary to disease or suppression of the hypothalamic-pituitary axis) mineralocorticoid function is preserved while there may be deficiency of hormones other than ACTH, notably LH/FSH and TSH |
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What are the main actions of cortisol?
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Facilitates gluconeogenesis and lipolysis
Inhibiting insulin secretion Anti-inflammatory actions Immune modulating effects Augmenting vascular reacitivity to vasoconstrictors Promoting catecholamine synthesis Retarding bone growth |
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What are the main causes of primary adrenal insufficiency?
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Chronic conditions
-autoimmune adrenalitis (Addison's) -infection (TB, HIV, fungal) -infiltrating diseases (sarcoid, amyloid, metastatic cancer) -surgical resection of both adrenals -drug toxicity (etomidate, ketoconazole, rifampicin) -Congenital adrenal hyperplasia Acute conditions -hemorrhage |
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What are the main causes of secondary adrenal insufficiency
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Chronic
-chronic steroid use (ACTH deficiency) -pituitary tumor, surgery, irradiation -postpartum pituitary necrosis (Sheehan's syndrome) -Traumatic brain injury -Empty sella syndrome -infiltrative disease of the pituitary Acute -pituitary apoplexy -Sheehan's syndrome -TBI -Relative adrenal insufficiency (inability to mount an adequate aCTH and cortisol response to sepsis, hepatic, failure, severe acute pancreatitis, trauma |
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What is Waterhouse-Friderichsen syndrome?
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Bilateral adrenal hemorrhage secondary to meningococcal sepsis.
Similar syndrome can be seen with other bacteria |
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How much exogenous glucocorticoid does it take to cause reduced adrenal responsiveness and possible atrophy?
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-Supraphysiologic doses for more than 3 weeks (hydrocortisone 30mg, prednisone 7.5mg or dexamethasone 0.75mg daily)
-As little as 5 days is required if the daily dose exceeds the equivalent of 20mg prednisone |
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How common is functional adrenal insufficiency in patients with septic shock
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More than 50%
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Describe adrenal crisis
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Refractory hypotension
Abdominal pain especially with adrenal hemorrhage or infarction |
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How do you confirm hypoadrenalism?
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-AM cortisol level >400nmol/L excludes the diagnosis, <80nmol/L is diagnostic
-random cortisol level >900nmol/L excludes the diagnosis, <400nmol/L is suggestive Levels between require confirmation with ACTH stimulation test: -baseline cortisol -Administer ACTH 250mg IV bolus -Repeat cortisol level at 30 minutes -Cortisol level >550nmol/L is normal -Cortisol increment <250nmol/L is diagnostic in critically ill patients |
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Can you begin treatment with corticosteroids before doing the ACTH test.
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Yes as long as you don't use hydrocortisone which would cross react in the cortisol assay. If this patient is not in adrenal crisis, use Dexamethasone 4mg IV q6-8h instead of hydrocortisone
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Outline your management of adrenal crisis
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Large bore IV access
Draw blood - electrolytes, glucose, plasma cortisol and ACTH Correct hypoglycemia Infuse 2-3 L of NS Hydrocortisone 100mg IV q6h Other supportive measures as indicated Search for and treat underlying precipitant |
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What chronic replacement therapy is indicated in patients with established adrenal insufficiency at baseline, during minor moderate illness, and for stressful procedures?
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-Chronic therapy is hydrocortisone 20mg PO qAM and 10mg PO q supper plus fludrocortisone per day
-During minor illness increase hydrocortisone 2-3 fold for the few days of illness -for a moderately stressful procedure like endoscopy or angio a single 100mg IV dose of hydrocortisone is given prior to the procedure |
