Endocrine Emergencies. Endocrine Emergencies. A 21 year old grad student Presents in DKA. How many causes of DKA are there? 5 Causes of DKA.

Transcription

1 Endocrine Emergencies Endocrine Emergencies Corey M. Slovis, M.D. Vanderbilt University Medical Center Metro Nashville Fire Department Nashville International Airport Nashville, TN DKA NKHC-Honk Hypoglycemia Hypo-Hyper Thyroid Hypo Adrenal Wernicke s and Pheo A 21 year old grad student Presents in DKA. How many causes of DKA are there? 5 Causes of DKA Infarction Infection Infant Indiscretion Insulin lack ph in DKA Acad Emerg Med 2003;10: Which is better, an ABG with arterial ph or just a venous ph? 200 ABGs and VpHs in DKA Patients ABG po 2 and pco 2 changed Rx in 2/200 High Art ph/v ph correlation (0.95)

2 Routinely Use VpH in DKA. How many therapies should you consider in DKA? Five Therapies to Consider in DKA Diabetes Care 2006;29: Volume v Insulin Potassium... Bicarbonate Phosphate Consensus statement of ADA The current standard of care 2,000 Diabetes Cases of DKA Therapy and Rationales in DKA Volume Enough to re-hydrate But don t wash out ketones Insulin Saturate receptors And keep saturated Potassium Avoid hyperkalemia early But avoid hypokalemia later Therapy and Rationales in DKA - 2 Bicarbonate Rarely needed Use for decompensation Phosphate Only cachectic patients Use for values below

3 VOLUME in DKA Deficits: 3-5 liters is usual deficit in mild-moderate DKA What is the best IV flow rate in DKA for the first 3 to 4 hours? 5-6 liters is usual fluid deficit in severe DKA JAMA 1989;262: Don t wash out all the Keto Acids. Let the Patient Metabolize Them Volume Therapy in DKA Begin Therapy: Bolus healthy patients with at least 1,000 cc of NSS (20 cc/kg) over first hour Stable Patients: NSS at 500 cc/hr x 4 hours Switch to NSS at 250 cc/hour Profound Dehydration: A patient in DKA has the following electrolytes: Glu = 660 BUN = 30 Cr = 1.2! What is the best IV fluid? NSS wide open until well perfused 18

4 NSS vs. _ NS NSS is the standard Use initially to volume load Consider _ NS if corrected serum sodium is Normal or Elevated The easiest way to correct for Na in DKA is v 2 meq _ Na for every 100mg/dl _ glucose Real Formula 1.6 _ Na/100 _ mg/dl glucose to _ Na/100 _ mg/dl > Glu = 660 Once Serum Glucose approaches 250 mg%:! Corrected Na = /100 glu _! Corrected Na = above 140 ( ) Use _ NS in this patient Switch to Glucose containing fluids (D 5 1/2 NS at cc/hr) 21 Cerebral Edema and DKA Increased morbidity and mortality Leading cause of death in pediatric DKA Does too much fluid in DKA cause cerebral edema? Lower ph and pco 2 increases incidence Aggressive fluids also implicated

5 NEJM 2001;344: children over 15 years Compared to matched and unmatched controls Cerebral Edema Associated with: _ CO 2 (11 vs ) _ BUN/Cr (27/1.5 vs. 21/ ) _ ph (7.06 vs ) NEJM 2001;344: The only therapeutic variable associated with cerebral edema in children with DKA was the administration of Bicarbonate. Low ph, low pco 2 levels and amount of dehydration also important You must: Insulin Provide a loading dose, and then Keep all receptor sites saturated Each unit of insulin moves about 4-5 grams of glucose into cell. Insulin Dosing Loading Dose 0.1 units/kg IV Push Maintenance Dose 0.1 units/kg per hour In general load adults, not children Should you insulin load adults and/or children? May overcome initial insulin resistance May acutely lower glucose J Emerg Med doi: More D 50 given to bolus group (??) but hypoglycemia not documented Bolus Not recommended in children

6 Potassium in DKA The average K deficit in DKA is 3-5 meq/kg IBW The ECG does not accurately predict hypokalemia A patient in DKA presents with K=5.1, ph =7.0, good urine output. How much KCl should be given in the first 4 hours? Potassium Dosing in DKA In general 10 meq/hr But Be sure K is in the DKA range of WNL KCL Replacement in First Hours of DKA Unexpected Death in DKA Hyperkalemia (above 5.3) DKA Kalemia ( ) Hypokalemia ( ) Severe HypoK (below 3.5) Hold K for 1 hr, recheck K KCL 10 meq/hr KCL 20 meq/hr Hold Insulin KCL meq/hr/constant ECG First hour or two when sick: Hyperkalemia Later while stabilizing : Hypokalemia

7 Refractory Acidosis in DKA A patient is treated for DKA and his glucose falls appropriately. His bicarbonate however, does not rise. First thoughts? Dead Gut Abscess/Sepsis A well-muscled football center presents in DKA. VS: BP=100/60 P=130 R=30 ABG s: ph = 6.9 pco 2 = 18 po 2 = 110 How much bicarbonate should be given? Potential Benefits Reverses Acidosis Improves Cardiac Output Increases Fibrillatory Threshold Improves Insulin Sensitivity Decreased Work of Breathing Bicarbonate Use Potential Risks Intracellular Acidosis Increased Ca, H+, K fluxes Hypokalemia, Tissue Hypoxia Hyperosmolarity, Hypernatremia Increased CO2 Generation, Respiratory Acidosis Decreased Length of Coma Paradoxical CSF Acidosis Recommendations on Bicarbonate It is generally agreed that: ph above 7.1 requires NO bicarbonate ph between rarely requires bicarbonate ph below 6.9 probably requires bicarbonate Rule 1: CO 2 freely Crosses BBB CO 2 CO 2 CO 2 CO 2

8 Rule 2: HCO 3 does not cross BBB HCO 3 Rule 3: Hyperventilation is based on venous ph not CSF ph. Bicarbonate is in equilibrium with C0 2 Giving HCO 3 raises CO 2 HCO 3 H 2 CO 3 CO 2 + H 2 O HCO 3 H 2 CO 3 CO 2 BBB Rules Baseline pco 2 crosses freely HCO 3 doesn t cross Ventilation rate (pco 2 ) determined by venous ph ph HCO 3 pco

9 CSF Acidosis - Giving Bicarbonate Push Bicarb ONLY For: ph HCO Unchanged Hyperkalemic emergency pco Impending cardiopulmonary arrest Hypoglycemia Why does every hypoglycemic patient s low blood glucose have to be ReExplained? Hypoglycemia ReExPLAIND Hypoglycemia (Renal) Re Ex P L A I N D Renal Exogenous Insulin/antihyperglycemics Pituitary Insufficiency Liver Alcohol, Addison s, Aspirin Infection, Insulinoma Neoplasm Drugs Decreased insulinase Decreased excretion Decreased caloric intake Increased number of infection

10 A 45 year old woman overdoses on her oral antihyperglycemia agent. IV glucose (repeat doses of D 50 ) fails to maintain her glucose RX? Decreased Hypoglycemic Episodes by a factor of 27 D 50 rarely required post octreotide Ann Emerg Med 2000;36: Stabilization was immediate Nonketotic Hyperosmolar Coma (NKHC, HONK) Not enough insulin to move glucose Enough insulin to block catabolic state Extreme glucose elevations Nonketotic Hyperosmolar Coma (NKHC) DKA NKHC Insulin levels very low may be normal Ketoacidosis profound minimal Glucose 600 1,000 HCO OSM Age young old Onset acute chronic Associated diseases rare common Seizures very rare common Coma rare common Mortality approaches % Treating NKHC Twice the volume deficit, but Treat _ as aggressively as DKA Tease with insulin, no drip DKA pts should never die, NKHC often do The 5 Most Common Endocrine Complaints Refractory Weakness Arrhythmias Altered Mental Status Fluid and Electrolyte Abnormalities

11 Refractory Shock NOT due to Sepsis AMI PE Drugs Hypothermia Endocrine - Metabolic Refractory = Endocrine Hypotension Hypothermia Bradycardia Tachycardia Arrhythmia Refractory Shock-Endocrine Metabolic Check Glucose Addison s Cachectic, Malabsorption Wernicke s Bradycardia +/or hypothermia Hypothyroidism History of Steroid use Addison s Hyperthyroidism Woman or Synthroid use Hypothyroidism What are some common ED complaints that should make us think: R/O Hyperthyroidism? Think Thyroid Disease ED Crocks Anxious and multiple nonspecific complaints Young, healthy but weak Amenorrhea but negative pregnancy test Diarrhea but otherwise healthy Palpations in exercising over-achiever

12 The one arrhythmia to always make you think of Hyperthyroidism is The most common cause of Hyperthyroidism in the ED is: Atrial Fibrillation with Rapid Ventricular Response Graves Disease Activation of Graves Disease is usually due to: When you see a Hyper or Hypo Thyroid Crisis, think: Discontinuing Medication Triggering Stress Hyperthyroidism R/O Triggering Stress Infection Pregnancy Trauma Recent surgical procedures High emotional stress Precipitating Cause! J Emerg Med 1996;14:

13 Am J Emerg Med 2001;19: Treatment of Hyperthyroidism ABC s NGT Block peripheral action Block synthesis Avoid relative hypoadrenalism Treatment of Hyperthyroidism ABC, NGT Thyroid Hormone Production Begin D5NSS at 200 cc/hr Intake of Organification Iodine Treatment of Hyperthyroidism Synthesis of Thyroid Hormone Release of Conversion Stimulus effects Active T4, T3 of T4 to T3 on the body Beta Blockers Beta Blockers block peripheral actions of Thyroid Hormone And also decrease peripheral conversion of T4 _ T3

14 Steroids PTU PTU blocks the formation of Active Thyroid Hormone And decreases T4 _ T3 conversion Treatment of Thyroid Storm Steroids support all organ system function Steroid help decrease T4 _ T3 conversion Steroids help borderline hypoadrenalism Iodine ABC/NGT Titrate Inderal 1 mg Q 3-5 min Begin PTU 750 mg PO Bolus with Steroids Administer Iodine Iodine in large doses blocks release of active T4 and T3 But: also stimulates new T3 and T4 formation If you give Iodine, block T3/T4 formation by first giving PTU Treatment of Hyperthyroidism Therapy IV D5NSS 200 cc/hr Titrate Inderal 1 mg Q5 PTU 750 mg PO Bolus Steroids (100mg Hydrocortisone) Iodine for Storm (1 gram Hypaque) Hypothyroidism

15 What patient types should make us consider Hypothyroidism? Hypothyroidism Chronic complainers Elderly with dementia CHF patient on diuretics with hyponatremia Digitalis toxicity even with decreasing dosage Hypertensive with repeat episodes of hypotension Fecal impaction, abdominal cramps, constipation Would minoxydil help? hair loss Most acute and some chronic ED presentations of hypothyroidism have a: precipitating cause: Find it! Myxedema A hypothyroid patient with: AMS + Significant Vital Sign Abnormalities Classic Myxedema Coma Patients: When should you consider myxedema coma? AMI with shock, poor response to pressors New Sick Sinus Syndrome, poor response to atropine Hypothermia in the spring, summer or fall Hypothermia that won t warm up AMS with sepsis

16 Myxedema Coma 5 Vital Signs BP: P: RR: Temp: O 2 sat: Hypotensive Bradycardic Hypercarbia Hypotensive Hypoxic Hypothyroid Patients Hypoventilate! 5 Heated O 2 N,G,T Synthroid Steroids Antibiotics Hypothermia Therapies to Consider Begin Therapy for Hypothermia Narcotic OD, Hypoglycemia, Wernicke s Hypothyroid Hypoadrenal/Hypothyroid Sepsis Treatment of Myxedema Coma Secure ABC s: High F i O 2 : Consider intubation Consider NGT: Beware hypoglycemia Thyroid Replacement: 400 ugm of Synthroid or 100 ugm T 3 Steroids: 100 mg IV of hydrocortisone, or decadron R/O underlying disease: R/O AMI, sepsis, head trauma, UTI etc. Hypothyroidism = Hyponatremia Hypothyroid = Hypoadrenal

17 Case 16 A hypothyroid asthmaticwith AIDS presents with purpuric lesionson his chest. Meds include coumadin. How many clues to this endocrine disease? What medication is key to curing him? HypoAdrenalism Adrenal Hormones Salt Water Energy Drink Aldosterone: Salt and Water Retention Cortisol: Energy Pressor Response Consider Adrenal Insufficiency Asthmatics (or history of steroid use) AIDS (infiltrative disease with MAI) Myxedema (or any endocrine disease) Meningiococcemia and Fulminant Sepsis Any Refractory Shock Patient - BP - P - Temp Consider Adrenal Insufficiency In any Hyperkalemic patient without renal failure In any Hypotensive patient not responding to volume or pressors In any Hypothermic patient not rewarming Treatment of Hypoadremalism Volume Glucose Sodium Steroids Diagnosis

18 Therapy of Adrenal Insufficiency Secure ABCs O 2, Volume, Na (D 5 NSS, cc/hr) NGT Glucose (D 5 NSS, cc/hr) Draw Red Top Label time drawn Therapy of Adrenal Insufficiency Steroids 6 mg Decadron ugm Corticotropin Find Cause R/O infection, infarction Redraw red top in min Diagnosing Addison s Disease Cosyntropin Stimulation Test Draw red top tube* Give 6 mg Decadron And 250 ugm Corticotropin Diagnosis of Hypoadrenalism Failure of cortisol level to rise to 20 ugm/dl, or at least double. Draw second red top min later* See if Cortisol level! 20 (or doubles) * Label Times!! Arch Surg 2008;143:67-71 Retrospective study of Trauma pts Etomidate use correlated with: Increased need for vasopressors Related adrenal insufficiency Ann Emerg Med Etomidate clearly depresses cosyntropin response Cortisol Levels remain unchanged Some recommend concurrent steroid administration Be careful with repeat dosing

19 Wernickes: The Classic Triad Wernicke s Encephalopathy Ataxia Ocular findings (nystagmus or LR-6 palsy) Encephalopathy Always Consider Wernicke s What are the 5 Groups to always consider giving Thiamine? Chronic Alcoholics Chronic Malnutrition Chronic Malabsorption Anorexia Nervosa Hyperemesis Gravidara Give Thiamine Ann Emerg Med 1989;18: Give 100 mg IV Thiamine to ALL cachetic or malnourished patients, even if not an alcoholic No Toxicity IV Push!

20 J Neurol, Neurosurg, and Psych 1986;49: Wernickes: Less Common Pentad Coma Miosis Hypotension Bradycardia Hypothermia A medical student faints while urinating. His BP is 300/200 and he is sweating, but 5 minutes later is 120/70. Pheo = Epinephrine Surges The Classic Triad of Pheos What three symptoms should make you think of pheochromocytoma? Episodic with and Headache Palpitations Sweating

21 Pheochromocytoma Symptoms Paroxysmal Hypertension Think Pheo Almost always paroxysmal Often last only a few minutes Rarely more than 1 hour Reoccurs in days, weeks, or months Hypertension in Pheo s 50:50 Summary Hypertension is the number 1 symptom BUT 50% have chronic Hypertension + Paroxysmal 50% have WNL Blood Pressure + Paroxysmal Bolus Patients in DKA Refractory = Endocrine Think Precipitating Causes Sepsis = R/o Endocrine Give Thiamine More