Ace844

"mediccjh," I hope that this post helps you with some more info. You can also check out this link to a similar scenario in which Right sided heart failure was discussed in detail, here's the link: http://www.emtcity.com/phpBB2/viewtopic.php?t=528. Based on the little you mentioned in your scenario, we know/assume the following: 1.) The patient has a PMH of CHF, of at this point unknown etiology. 2.) The patient takes "inhalers" A.K.A: beta agonists for an as of yet unknown respiratory reason. 3.) That the patient is complaining of resp distress and has the clinical signs/sx's of CHF/Dyspenic syndrome... 4.) The patient is in A-Fib on your "monitor" 5.) The patient has ascities which as previously mentioned here is a sign/sx of underlying Liver dysfunction as caused by "alcholic liver", hepatitis, etc....This may have been what caused the patients CHF (i.e.: portal HTn, hypoalbuminemia) in the first place...but one can never be sure without access to MR'sand a comprehensive PMHX.. 6.) It can be reasonably assumed with the PE findings of HJR, and ascities, that this patient also has a component of portal hypertension. Most of your questions should be answered from the link I posted but I'd like to make a few additional points. 1.) Some of the PE signs/sx's you posted are the following: HJR, which stands for Hepato Jugular Reflux, and two which you didn't mention. These are JVP measurement, and Kussmaul's sign. These are assessed as follows: Close examination of the neck veins is very important. Whereas the external jugular vein gives a general idea of the height of the venous waves, the internal jugular vein is used for analysis of venous pressure and the venous waveform because it acts as an open venous conduit to the right atrium (except in cases of superior vena cava obstruction). (Hepato-Jugular reflux test) The jugular veins are usually examined with the patient reclining at 45°, whereby the venous column in normal persons is just below the clavicles. The venous column can briefly be elevated above the clavicle by firm pressure of the hand on the abdomen (the hepatojugular reflux), but in normal persons it will fall below the clavicle in a few seconds while maintaining abdominal pressure as the compliant right ventricle increases its stroke volume by means of the Frank-Starling mechanism. In superior vena cava obstruction, constrictive pericarditis, restrictive cardiomyopathy, or severe heart failure, the jugular venous pressure may be sufficiently elevated to make detection of the top of the venous column impossible. In these circumstances, the patient should be examined while sitting upright or standing. Change in the height of the venous waves in response to abdominal compression gives considerable information about the right side of the heart. The venous column rises and remains elevated while abdominal pressure is maintained in the presence of a dilated, poorly compliant right ventricle; in constrictive pericarditis or pericardial tamponade; and with obstructed right ventricular filling by tricuspid stenosis or right atrial tumor. Kussmaul's sign should be sought, in which, under the same circumstances that produce a hepatojugular reflux abnormality, the venous column in the neck rises rather than falls with inspiration. In normal inspiration, lowered intrathoracic pressure draws blood from the periphery into the vena cava. The normally compliant right ventricle accommodates and expels this blood by means of the Frank-Starling mechanism. Kussmaul's sign is also present in obstructive airway disease. Finally, the character and magnitude of the venous waves can be analyzed. The a and v waves are increased in pulmonary hypertension. Giant a waves (cannon waves) are seen in atrial ventricular dissociation. The a wave disappears in atrial fibrillation and is accentuated in states of poor right ventricular compliance (eg, pulmonary hypertension, pulmonic valve stenosis). The v wave becomes very prominent if tricuspid regurgitation is present. Tricuspid regurgitation also often produces significant hepatomegaly, with easily palpable systolic pulsation of the liver due to the regurgitant v wave swelling the liver during right ventricular systole. The accompanying marked venous hypertension sometimes leads to cardiac cirrhosis and ascites. In cardiac tamponade, the x descent is steep. In states of poor right ventricular compliance, the y descent following ventricular systole is very abrupt because the elevated column of venous blood rushes into the right ventricle on opening of the tricuspid valve, only to stop abruptly as the rigid right ventricular wall (in restrictive myopathy) or the pericardium (in constrictive pericarditis) arrests the inflow. Now you mentioned that your patient was in "a-fib" on your monitor but you are You could do a modified 12 lead by moving your MCL-1 around the "V" leads and this would give you a " 12 lead perspective" on your patients with a 3 lead monitor. Hope this helps, Ace844

Dear USAF, Hmm, can't decide if your being facetious, or trying to goad me into a largly hostile response.....As far as cutting and pasting, yeah I do it, mostly to make a point...seems you do it alot as well...yet, I haven't accused you of being in the same league with another poster on these forums with whom you've had disagreements with. Also, In my posts, I agreed with "asys", and moved on to further posts examples of what "some" of us we're already saying. Also, with what you posted, you "agreed" with my responses...so does that mean you are calling yourself wrong as well???? :?: :!: :arrow: At this point "Steve", you seem to very much be the proverbial "pot calling the kettle....." So what's/why the issue? As far as being new..yeah I'm a rookie, with 10 or so years of urban 911 (with some tranfer stuff mixed in)...worth of experience...newer than some, more experienced than others....it seems?!! :wink: :twisted: It seems I that I learn new things in medicine all of the time, sometimes here, or even other places..but at no point do I porport to be the end all be all...do you>!?!?!?!!?!? :roll: :idea: Still i have yet to marginalize you or your posting efforts....so thus I look forward to your response or flames...whichever may come!! Out here, Ace844

Hi All, To further illustrate another side to this, I'd like to take a second to present another possibility to the group. I'll keep this very general and take some expansion liberties to make a point for the large picture purpose of this post. So here it goes. Ok, so since we are talking about Sz D/O's in Diabetic's; lets say that you arrive on a scene to find a patient whom has a PMH of IDDM, and is actively seizing. Also lets say that since as "Asysin2leads" has pointed out in the last post that we are all of 2 camps. Camp A in this case stabilizes the patient via giving Lorazapam, (or which ever anti-seizure med your protocols allow you to use), and that the seizure breaks, lets all so say that after or before the med was given that IV access was sucessfully obtained, and then the patient got a full assessment including a FSBS/BGL, then Group A treats whatever underlying disorders they may find....... Now conversely, we go to the second "group", Group B. Group B (Which may or may not be as protrayed by "Asysin2leads", whom assumes that you haven't had the opportunity to actually treat a seizure before reading about it in a book some place) Arrives to find the same patient and immediately upon learning the patient is a diabetic, assumes that because the patient is a Diabetic, or upon a FSBS/BGL reading that is low, assumes this is a primary Diabetes related disorder only. So thus this "group", either with or without Iv access gives either Glucagon, or D50, (Or what ever sugar "boosting" solution you prefer, or protocol allows. This may or may not stop the seizure in which case "Group B" would then hypothetically and Hopefully search for other causes and also give Benzo's to break the seizure. The problem with these above approaches which the "groups" fail to take into account is as follows..... A.) As referenced by "Asysin2leads" in their post, that "Group B" has unequal experience from "Group A" and that this may be abit too much of a generality. B.) Having said that "Group A" I believe is taking the better approach because they are treating their "patient" with the awareness that there are other things that cause a Seizure than just hypoglycemia in a diabetic patient. They treat the seizure and once the Airway and life threatening Seizure is "stopped", they then proceed to assess and treat all further life threats, and electrolyte disorders C.)As "buddha", and to add to his statement of, The fact that a patient who is or has seized, will most likely be hypoglycemic as all of that motor activity "burns" alot of the glucose reserves in the body!!! :idea: :!: D.) The fact that one of our "groups" fails to understand that indescrimenately giving "Glucose" to a patient can very be harmful, regardless of PMH. A quick example of this off the top of my head.....Let's say that in the above and the scenario which caused all of these posts the following happened. 1.) Group A did as posted above, and found that their patient had a low BGL level but didn't aggressively correct it because they foud Objective assessment evidence of a "intercrainal bleed"....Now had they given this patient "a bolus of D50/Glucagon/etc...." then they would have significantly worsened this patients out come and caused harm by increasing the "bleed" situation. 2.) Group B provides a different Rx, approach and give "sugar" then when the seizure doesn't stop, gives some Benzo's to stop the patients seizing, and also begins to think of other causes.....Which incidentally provides them with the problem of having administered a med to a patient which caused their condition to worsen, and is not something they can "take back." Had Group B appraoched the patient as they have been trained since the enception of their EMS career, and treated the immediate life threats first, (In this case the lack of a patent airway, and the seizure activity) as well as doing a comprehensive thorough assessment, they would have found that this patient had a different reason to "seize" other than just assuming it was their "Diabetes" that caused it. Also they would have provented themselves from making the "error" of giving a med to a patient which would cause their condition to worsen (This being the "true underlying cause" which wasn't the one they assumed and immediately treated), rather they treated based on incomplete info. and disregarding other equally important possibilities. E.) As "Buddah" noted it is very "hard" to get a IV in an "actively seizing" patient. The Take home lessons are these:: ** ASSESS, ASSESS, ASSESS, DON'T ASSUME ANYTHING!! ** TREAT ALL IMMEDIATE LIFE THREATS WHILE SEARCHING FOR UNDERLYING ETIOLOGY AT THE SAME TIME!! ** ONLY AFTER YOU HAVE RULED OUT ALL OTHER DISORDERS AND ARE LEFT WITH 1 OR 2 AS THE ONLY DDX'S LEFT THEN TREAT THESE ** KNOW THE MEDS YOU ARE ADMINISTERING AND WHAT THE PEARLS AND PITFALLS OF THEM ARE!! ** WHEN IN DOUBT ASK QUESTIONS !! Hope this helps, Out here, Ace844

Hi "ardolphin26", Just incase you were unaware, when the poster was referring to Glucagon they were referring to the IM medicine, not the "sugar in a tube" to which you were referring. here's more info on glucagon in case you don't have access and here's a link to check as well. http://www.drugs.com/PDR/Glucagon_for_Inje...rgency_Kit.html Hope this helps, Ace844 PDR Drug information for Glucagon for Injection Vials and Emergency Kit Manufacturer: Lilly INFORMATION FOR THE PHYSICIAN DESCRIPTION Glucagon for Injection (rDNA origin) is a polypeptide hormone identical to human glucagon that increases blood glucose and relaxes smooth muscle of the gastrointestinal tract. Glucagon is synthesized in a special non-pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagon. Glucagon is a single-chain polypeptide that contains 29 amino acid residues and has a molecular weight of 3,483. The empirical formula is C 153 H 225 N 43 O 49 S. The primary sequence of glucagon is shown below. Crystalline glucagon is a white to off-white powder. It is relatively insoluble in water but is soluble at a pH of less than 3 or more than 9.5. Glucagon is available for use intravenously, intramuscularly, or subcutaneously in a kit that contains a vial of sterile glucagon and a syringe of sterile diluent. The vial contains 1 mg (1 unit) of glucagon and 49 mg of lactose. Hydrochloric acid may have been added during manufacture to adjust the pH of the glucagon. One International Unit of glucagon is equivalent to 1 mg of glucagon. 1 The diluent syringe contains 12 mg/mL of glycerin, water for injection, and hydrochloric acid. CLINICAL PHARMACOLOGY Glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose. Glucagon administered through a parenteral route relaxes smooth muscle of the stomach, duodenum, small bowel, and colon. Pharmacokinetics Glucagon has been studied following intramuscular, subcutaneous, and intravenous administration in adult volunteers. Administration of the intravenous glucagon showed dose proportionality of the pharmacokinetics between 0.25 and 2.0 mg. Calculations from a 1 mg dose showed a small volume of distribution (mean, 0.25 L/kg) and a moderate clearance (mean, 13.5 mL/min/kg). The half-life was short, ranging from 8 to 18 minutes. Maximum plasma concentrations of 7.9 ng/mL were achieved approximately 20 minutes after subcutaneous administration ( see Figure 1A ). With intramuscular dosing, maximum plasma concentrations of 6.9 ng/mL were attained approximately 13 minutes after dosing. Glucagon is extensively degraded in liver, kidney, and plasma. Urinary excretion of intact glucagon has not been measured. Pharmacodynamics In a study of 25 volunteers, a subcutaneous dose of 1 mg glucagon resulted in a mean peak glucose concentration of 136 mg/dL 30 minutes after injection ( see Figure 1B ). Similarly, following intramuscular injection, the mean peak glucose level was 138 mg/dL, which occurred at 26 minutes after injection. No difference in maximum blood glucose concentration between animal-sourced and rDNA glucagon was observed after subcutaneous and intramuscular injection. INDICATIONS AND USAGE For the treatment of hypoglycemia: Glucagon is indicated as a treatment for severe hypoglycemia. Because patients with type 1 diabetes may have less of an increase in blood glucose levels compared with a stable type 2 patient, supplementary carbohydrate should be given as soon as possible, especially to a pediatric patient. For use as a diagnostic aid: Glucagon is indicated as a diagnostic aid in the radiologic examination of the stomach, duodenum, small bowel, and colon when diminished intestinal motility would be advantageous. Glucagon is as effective for this examination as are the anticholinergic drugs. However, the addition of the anticholinergic agent may result in increased side effects. CONTRAINDICATIONS Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. WARNINGS Glucagon should be administered cautiously to patients with a history suggestive of insulinoma, pheochromocytoma, or both. In patients with insulinoma, intravenous administration of glucagon may produce an initial increase in blood glucose; however, because of glucagon's hyperglycemic effect the insulinoma may release insulin and cause subsequent hypoglycemia. A patient developing symptoms of hypoglycemia after a dose of glucagon should be given glucose orally, intravenously, or by gavage, whichever is most appropriate. Exogenous glucagon also stimulates the release of catecholamines. In the presence of pheochromocytoma, glucagon can cause the tumor to release catecholamines, which may result in a sudden and marked increase in blood pressure. If a patient develops a sudden increase in blood pressure, 5 to 10 mg of phentolamine mesylate may be administered intravenously in an attempt to control the blood pressure. Generalized allergic reactions, including urticaria, respiratory distress, and hypotension, have been reported in patients who received glucagon by injection. PRECAUTIONS General-- Glucagon is effective in treating hypoglycemia only if sufficient liver glycogen is present. Because glucagon is of little or no help in states of starvation, adrenal insufficiency, or chronic hypoglycemia, hypoglycemia in these conditions should be treated with glucose. Information for Patients-- Refer patients and family members to the attached Information for the User for instructions describing the method of preparing and injecting glucagon. Advise the patient and family members to become familiar with the technique of preparing glucagon before an emergency arises. Instruct patients to use 1 mg (1 unit) for adults and 1/2 the adult dose (0.5 mg) [0.5 unit] for pediatric patients weighing less than 44 lb (20 kg). Patients and family members should be informed of the following measures to prevent hypoglycemic reactions due to insulin: Reasonable uniformity from day to day with regard to diet, insulin, and exercise. Careful adjustment of the insulin program so that the type (or types) of insulin, dose, and time (or times) of administration are suited to the individual patient. Frequent testing of the blood or urine for glucose so that a change in insulin requirements can be foreseen. Routine carrying of sugar, candy, or other readily absorbable carbohydrate by the patient so that it may be taken at the first warning of an oncoming reaction. To prevent severe hypoglycemia, patients and family members should be informed of the symptoms of mild hypoglycemia and how to treat it appropriately. Family members should be informed to arouse the patient as quickly as possible because prolonged hypoglycemia may result in damage to the central nervous system. Glucagon or intravenous glucose should awaken the patient sufficiently so that oral carbohydrates may be taken. Patients should be advised to inform their physician when hypoglycemic reactions occur so that the treatment regimen may be adjusted if necessary. Laboratory Tests-- Blood glucose determinations should be obtained to follow the patient with hypoglycemia until patient is asymptomatic. Carcinogenesis, Mutagenesis, Impairment of Fertility-- Because glucagon is usually given in a single dose and has a very short half-life, no studies have been done regarding carcinogenesis. In a series of studies examining effects on the bacterial mutagenesis (Ames) assay, it was determined that an increase in colony counts was related to technical difficulties in running this assay with peptides and was not due to mutagenic activities of the glucagon. Reproduction studies have been performed in rats at doses up to 2 mg/kg glucagon administered two times a day (up to 40 times the human dose based on body surface area, mg/m 2 ) and have revealed no evidence of impaired fertility. Pregnancy--Pregnancy Category B-- Reproduction studies have not been performed with recombinant glucagon. However, studies with animal-sourced glucagon were performed in rats at doses up to 2 mg/kg glucagon administered two times a day (up to 40 times the human dose based on body surface area, mg/m 2 ), and have revealed no evidence of impaired fertility or harm to the fetus due to glucagon. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed. Nursing Mothers- - It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when glucagon is administered to a nursing woman. If the drug is excreted in human milk during its short half-life, it will be hydrolyzed and absorbed like any other polypeptide. Glucagon is not active when taken orally because it is destroyed in the gastrointestinal tract before it can be absorbed. Pediatric Use- - For the treatment of hypoglycemia: The use of glucagon in pediatric patients has been reported to be safe and effective. 2-6 For use as a diagnostic aid: Effectiveness has not been established in pediatric patients. ADVERSE REACTIONS Severe adverse reactions are very rare, although nausea and vomiting may occur occasionally. These reactions may also occur with hypoglycemia. Generalized allergic reactions have been reported ( see WARNINGS ). In a three month controlled study of 75 volunteers comparing animal-sourced glucagon with glucagon manufactured through rDNA technology, no glucagon-specific antibodies were detected in either treatment group. OVERDOSAGE Signs and Symptoms-- If overdosage occurs, nausea, vomiting, gastric hypotonicity, and diarrhea would be expected without causing consequential toxicity. Intravenous administration of glucagon has been shown to have positive inotropic and chronotropic effects. A transient increase in both blood pressure and pulse rate may occur following the administration of glucagon. Patients taking (beta)-blockers might be expected to have a greater increase in both pulse and blood pressure, an increase of which will be transient because of glucagon's short half-life. The increase in blood pressure and pulse rate may require therapy in patients with pheochromocytoma or coronary artery disease. When glucagon was given in large doses to patients with cardiac disease, investigators reported a positive inotropic effect. These investigators administered glucagon in doses of 0.5 to 16 mg/hour by continuous infusion for periods of 5 to 166 hours. Total doses ranged from 25 to 996 mg, and a 21-month-old infant received approximately 8.25 mg in 165 hours. Side effects included nausea, vomiting, and decreasing serum potassium concentration. Serum potassium concentration could be maintained within normal limits with supplemental potassium. The intravenous median lethal dose for glucagon in mice and rats is approximately 300 mg/kg and 38.6 mg/kg, respectively. Because glucagon is a polypeptide, it would be rapidly destroyed in the gastrointestinal tract if it were to be accidentally ingested. Treatment-- To obtain up-to-date information about the treatment of overdose, a good resource is your certified Regional Poison Control Center. Telephone numbers of certified poison control centers are listed in the Physicians' Desk Reference (PDR) . In managing overdosage, consider the possibility of multiple drug overdoses, interaction among drugs, and unusual drug kinetics in your patient. In view of the extremely short half-life of glucagon and its prompt destruction and excretion, the treatment of overdosage is symptomatic, primarily for nausea, vomiting, and possible hypokalemia. If the patient develops a dramatic increase in blood pressure, 5 to 10 mg of phentolamine mesylate has been shown to be effective in lowering blood pressure for the short time that control would be needed. Forced diuresis, peritoneal dialysis, hemodialysis, or charcoal hemoperfusion have not been established as beneficial for an overdose of glucagon; it is extremely unlikely that one of these procedures would ever be indicated. DOSAGE AND ADMINISTRATION General Instructions for Use: The diluent is provided for use only in the preparation of glucagon for parenteral injection and for no other use. Glucagon should not be used at concentrations greater than 1 mg/mL (1 unit/mL). Reconstituted glucagon should be used immediately. Discard any unused portion. Reconstituted glucagon solutions should be used only if they are clear and of a water-like consistency. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration. Directions for Treatment of Severe Hypoglycemia: Severe hypoglycemia should be treated initially with intravenous glucose, if possible. If parenteral glucose can not be used, dissolve the lyophilized glucagon using the accompanying diluting solution and use immediately. For adults and for pediatric patients weighing more than 44 lb (20 kg), give 1 mg (1 unit) by subcutaneous, intramuscular, or intravenous injection. For pediatric patients weighing less than 44 lb (20 kg), give 0.5 mg (0.5 unit) or a dose equivalent to 20-30 µg/kg. 2-6 Discard any unused portion. An unconscious patient will usually awaken within 15 minutes following the glucagon injection. If the response is delayed, there is no contraindication to the administration of an additional dose of glucagon; however, in view of the deleterious effects of cerebral hypoglycemia emergency aid should be sought so that parenteral glucose can be given. After the patient responds, supplemental carbohydrate should be given to restore liver glycogen and to prevent secondary hypoglycemia. Directions for Use as a Diagnostic Aid: Dissolve the lyophilized glucagon using the accompanying diluting solution and use immediately. Discard any unused portion. The doses in the following table may be administered for relaxation of the stomach, duodenum, and small bowel, depending on the onset and duration of effect required for the examination. Since the stomach is less sensitive to the effect of glucagon, 0.5 mg (0.5 units) IV or 2 mg (2 units) IM are recommended. Dose Route of Administration Time of Onset of Action Approximate Duration of Effect 0.25-0.5 mg IV 1 minute 9-17 minutes (0.25-0.5 units) 1 mg (1 unit) IM 8-10 minutes 12-27 minutes 2 mg * (2 units) IV 1 minute 22-25 minutes 2 mg * (2 units) IM 4-7 minutes 21-32 minutes *Administration of 2 mg (2 units) doses produces a higher incidence of nausea and vomiting than do lower doses. For examination of the colon, it is recommended that a 2 mg (2 units) dose be administered intramuscularly approximately 10 minutes prior to the procedure. Colon relaxation and reduction of patient discomfort may allow the radiologist to perform a more satisfactory examination. HOW SUPPLIED Glucagon Emergency Kit for Low Blood Sugar (Glucagon for Injection [rDNA origin]) (MS8031): 1 mg (1 unit)--(VL7529), with 1 mL of diluting solution (Hyporet® * HY7530) (1s) NDC 0002-8031-01 Glucagon Diagnostic Kit (Glucagon for Injection [rDNA ori- gin]) (MS8085): 1 mg (1 unit)--(VL7529), with 1 mL of diluting solution (Hyporet® * HY7530) (1s) NDC 0002-8085-01 (available in US market only). -------------------------------------------------------------------------------- *Hyporet® (disposable syringe, Lilly). Stability and Storage: Before Reconstitution --Vials of Glucagon, as well as the Diluting Solution for Glucagon, may be stored at controlled room temperature 20° to 25°C (68° to 77°F)[see USP]. The USP defines controlled room temperature by the following: A temperature maintained thermostatically that encompasses the usual and customary working environment of 20° to 25°C (68° to 77°F); that results in a mean kinetic temperature calculated to be not more than 25°C; and that allows for excursions between 15° and 30°C (59° and 86°F) that are experienced in pharmacies, hospitals, and warehouses. After Reconstitution --Glucagon for Injection (rDNA origin) should be used immediately. Discard any unused portion. REFERENCES Drug Information for the Health Care Professional. 18th ed. Rockville, Maryland: The United States Pharmacopeial Convention, Inc; 1998; I:1512. Gibbs et al: Use of glucagon to terminate insulin reactions in diabetic children. Nebr Med J 1958;43:56-57. Cornblath M, et al: Studies of carbohydrate metabolism in the newborn: Effect of glucagon on concentration of sugar in capillary blood of newborn infant. Pediatrics 1958;21:885-892. Carson MJ, Koch R: Clinical studies with glucagon in children. J Pediatr 1955;47:161-170. Shipp JC, et al: Treatment of insulin hypoglycemia in diabetic campers. Diabetes 1964;13:645-648. Aman J, Wranne L: Hypoglycemia in childhood diabetes II: Effect of subcutaneous or intramuscular injection of different doses of glucagon. Acta Pediatr Scand 1988;77:548-553. Literature revised April 27, 2001 PA 2282 AMP Copyright © 1999, 2001, Eli Lilly and Company. All rights reserved. INFORMATION FOR THE USER GLUCAGON FOR INJECTION (rDNA ORIGIN) BECOME FAMILIAR WITH THE FOLLOWING INSTRUCTIONS BEFORE AN EMERGENCY ARISES. DO NOT USE THIS KIT AFTER DATE STAMPED ON THE BOTTLE LABEL. IF YOU HAVE QUESTIONS CONCERNING THE USE OF THIS PRODUCT, CONSULT A DOCTOR, NURSE OR PHARMACIST. Make sure that your relatives or close friends know that if you become unconscious, medical assistance must always be sought. Glucagon may have been prescribed so that members of your household can give the injection if you become hypoglycemic and are unable to take sugar by mouth. If you are unconscious, glucagon can be given while awaiting medical assistance. Show your family members and others where you keep this kit and how to use it. They need to know how to use it before you need it. They can practice giving a shot by giving you your normal insulin shots. It is important that they practice. A person who has never given a shot probably will not be able to do it in an emergency. IMPORTANT Act quickly. Prolonged unconsciousness may be harmful. These simple instructions will help you give glucagon successfully. Turn patient on his/her side to prevent patient from choking. The contents of the syringe are inactive. You must mix the contents of the syringe with the glucagon in the accompanying bottle before giving injection. (See DIRECTIONS FOR USE below.) Do not prepare Glucagon for Injection until you are ready to use it. WARNING: THE PATIENT MAY BE IN A COMA FROM SEVERE HYPERGLYCEMIA (HIGH BLOOD GLUCOSE) RATHER THAN HYPOGLYCEMIA. IN SUCH A CASE, THE PATIENT WILL NOT RESPOND TO GLUCAGON AND REQUIRES IMMEDIATE MEDICAL ATTENTION. INDICATIONS FOR USE Use glucagon to treat insulin coma or insulin reaction resulting from severe hypoglycemia (low blood sugar). Symptoms of severe hypoglycemia include disorientation, unconsciousness, and seizures or convulsions. Give glucagon if (1) the patient is unconscious (2) the patient is unable to eat sugar or a sugar-sweetened product (3) the patient is having a seizure, or (4) repeated administration of sugar or a sugar-sweetened product such as a regular soft drink or fruit juice does not improve the patient's condition. Milder cases of hypoglycemia should be treated promptly by eating sugar or a sugar-sweetened product. (See INFORMATION ON HYPOGLYCEMIA below for more information on the symptoms of hypoglycemia.) Glucagon is not active when taken orally. DIRECTIONS FOR USE TO PREPARE GLUCAGON FOR INJECTION Remove the flip-off seal from the bottle of glucagon. Wipe rubber stopper on bottle with alcohol swab. Remove the needle protector from the syringe, and inject the entire contents of the syringe into the bottle of glucagon. DO NOT REMOVE THE PLASTIC CLIP FROM THE SYRINGE. Remove syringe from the bottle. Swirl bottle gently until glucagon dissolves completely. GLUCAGON SHOULD NOT BE USED UNLESS THE SOLUTION IS CLEAR AND OF A WATER-LIKE CONSISTENCY. TO INJECT GLUCAGON Use Same Technique as for Injecting Insulin Using the same syringe, hold bottle upside down and, making sure the needle tip remains in solution, gently withdraw all of the solution (1 mg mark on syringe) from bottle. The plastic clip on the syringe will prevent the rubber stopper from being pulled out of the syringe; however, if the plastic plunger rod separates from the rubber stopper, simply reinsert the rod by turning it clockwise. The usual adult dose is 1 mg (1 unit). For children weighing less than 44 lb (20 kg), give 1/2 adult dose (0.5 mg). For children, withdraw 1/2 of the solution from the bottle (0.5 mg mark on syringe). DISCARD UNUSED PORTION. USING THE FOLLOWING DIRECTIONS, INJECT GLUCAGON IMMEDIATELY AFTER MIXING. Cleanse injection site on buttock, arm, or thigh with alcohol swab. Insert the needle into the loose tissue under the cleansed injection site, and inject all (or ½ for children weighing less than 44 lb) of the glucagon solution. THERE IS NO DANGER OF OVERDOSE. Apply light pressure at the injection site, and withdraw the needle. Press an alcohol swab against the injection site. Turn the patient on his/her side. When an unconscious person awakens, he/she may vomit. Turning the patient on his/her side will prevent him/her from choking. FEED THE PATIENT AS SOON AS HE/SHE AWAKENS AND IS ABLE TO SWALLOW. Give the patient a fast-acting source of sugar (such as a regular soft drink or fruit juice) and a long-acting source of sugar (such as crackers and cheese or a meat sandwich). If the patient does not awaken within 15 minutes, give another dose of glucagon and INFORM A DOCTOR OR EMERGENCY SERVICES IMMEDIATELY. Even if the glucagon revives the patient, his/her doctor should be promptly notified. A doctor should be notified whenever severe hypoglycemic reactions occur. INFORMATION ON HYPOGLYCEMIA Early symptoms of hypoglycemia (low blood glucose) include: sweating dizziness palpitation tremor hunger restlessness tingling in the hands, feet, lips, or tongue lightheadedness inability to concentrate headache drowsiness sleep disturbances anxiety blurred vision slurred speech depressed mood irritability abnormal behavior unsteady movement personality changes If not treated, the patient may progress to severe hypoglycemia that can include: disorientation unconsciousness seizures death The occurrence of early symptoms calls for prompt and, if necessary, repeated administration of some form of carbohydrate. Patients should always carry a quick source of sugar, such as candy mints or glucose tablets. The prompt treatment of mild hypoglycemic symptoms can prevent severe hypoglycemic reactions. If the patient does not improve or if administration of carbohydrate is impossible, glucagon should be given or the patient should be treated with intravenous glucose at a medical facility. Glucagon, a naturally occurring substance produced by the pancreas, is helpful because it enables the patient to produce his/her own blood glucose to correct the hypoglycemia. POSSIBLE PROBLEMS WITH GLUCAGON TREATMENT Severe side effects are very rare, although nausea and vomiting may occur occasionally. A few people may be allergic to glucagon or to one of the inactive ingredients in glucagon, or may experience rapid heart beat for a short while. If you experience any other reactions which are likely to have been caused by glucagon, please contact your doctor. STORAGE Before dissolving glucagon with diluting solution--Store the kit at controlled room temperature between 20° to 25°C (68° to 77°F). After dissolving glucagon with diluting solution--Should be used immediately. Discard any unused portion. Solutions should be clear and of a water-like consistency at time of use. Literature revised April 27, 2001 PA 2282 AMP Copyright © 1999, 2001, Eli Lilly and Company. All rights reserved. http://' target="_blank">

Hi all, "buddha", thanks for helping to illustrate the point here which is in short. Not always is the presenting symptom or underlying disorder the zebra in a herd of horses, but if you take all the horses away and are left with a zebra....then.... :roll: :idea: then your clue phone should ring!!! out here, Ace844

Steve, Out of curiousity, do you or any of the posters here use FEV1 as a clinical measure of how effective your Albuterol or combivent RX's are??? If not what do you use? Is it strictly subjective? Also, will you have an objective/subjective clinical measure in your study, if so what method will you use? Also as you noted for COPD and BOOP I have seen dramatic improvement with BIPAP/CPAP...just curious, that always asking ?'s and learning more EMS professional, Ace844

Buddah, Some things weren't meant to be shared man... Ace

Dear "John," You should perhaps read a previous thread that was posted, here's the "link"http://www.emtcity.com/phpBB2/viewtopic.ph...&highlight=...It should also be noted that there has 0 studies showing RSi's efficacy in an ER as well, so by your own logic they shouldn't do it there either.... Hope this helps... Ace

Hi All, To further muddy the waters here a bit, I also respectfully present for your consideration the possibility that not every patient who happens to be a diabetic and whom then develops seizure activity, who or what is to say that their seizure was caused by a diabetic disorder in the first place???!!!! :?: :idea: What about a comprehensive exam in this case especially!! :arrow: out here, Ace844

Hi All, Please reread my preceeding post. I think that it's important to note that the Active Seizure is the more life threatening event here, and if your patient is actively seizing, THEY ARE NOT BREATHING!!!! :idea: :idea: :roll: :!: Yes a diabetic needs their sugar imbalence corrected, but even a diabetic who is seizing that get D50 or Glucagon and continues to seize will VERY QUICKLY burn through that additional sugar, also the hypoxia will do as much or more brain/neuro damage than if it was a pure isolated hypoglycemic even....just my .02, IMHLO... Hope this helps.., Ace844

"RamVacEms", There is at least one absolute contraindication to O2 therepy and many more"relative" ones. The "absolute" is a paraquat, cumquat ingestion or suspicion there of. As far as the relative, well there are many... I posted a scenario either here or on the old board and I can't seem to find a link, so if anyone has it, I'd appreciate it if you'd help out and post it. Hope this helps, Ace844

USAF, Thganks for the O2 info., and double thanks for not posting Winter's formula...I think I would have had to leave my comp and go bang my head against the wall several times if you had..... "rid," I definately think we should allow this scientist to try out his theory on HIMSELF in realtime...perhaps we could even change the CO2 to be the actual percentage of atmospheric Nitrogen...I bet that'd make him happier, then we could even tape the whole thing and see how much "practicality" his research holds.... :twisted: :!: :idea: LOL Out here, Ace

You know your in Urban EMS provider when you sign off at the hospital with a patient and the Dispatcher kindly informs you that he has your next "Emergency" waiting for ya...and BTW could ya hurry it up so he can assign you the call cuz ur GONNA GET IT!!! Ace844

Hi All, Perhaps soemone could clarify for me....What is the issue with using both medicines as an initial treatment regime....Yes, I understand that you need to find, and treat the underlying etiology of the disorder. But truth of the matter is, most seizure patients ARE HYPOGLYCEMIC AS A RESULT OF THEIR SEIZURE ACTIVITY!!!! :wink: !! Yes, with diabetics, it is an important distinction to make, but only AFTER YOU'VE CORRECTED THE LIFE THREATENING DISORDERS FIRST!! Also, it is important to note that benzo's merely stop the motor activity end of the seizure and that if your patient is truely atatus seizing, their brain will most likely continue to seize after the benzos. I think that the benzo's should be given and simultaneously, a dex stick performed, and then D50/Glucagon, thiamine should be given as needed... Out here, Ace844

Hi all, I'll tell ya when we were deoming new 12 leads a service I was working at we used to have a routine. We'd take the monitor, at the time either an MRL, lp12, or zoll, and try them out on a real person, run the sims, harass the rep with questions, then toss it out the 2nd story window, roll it down a flight of stairs and then repeat the first step. third, we then trial it on real calls for awhile, then return it to the rep. Next we submit comments/concerns/complaints/etc...to the comapny and they take all of the preceeding and make a choice. I'll tell ya, if you wanna have a good time and perhaps have a camera handy.....do this and take pictures of the rep..too funny!!!!!!!! anywho, we ended up with the MRL and I really liked the features and easy expandability it offered. Ace

Ohhh....doggy!! :? So lets see, RID, USAF, Titinaelli and Rosen, as well as some mystery guests get together and make the ideal "medic" test...hmmm...why do I think that I'll be getting "the special test"??? anywho....bring, send it, can't wait to see how much this will hurt, can't be much worse than the sadist medic class I've been suffering through...oh and BTW, whats the award if we pass???? can't wait to see what you all bring to the table.. out here, Ace

I think EMS is an awesome profession...why right after I joined I gots to learns my lettas and mys numbas..now its all good...who cares what I wear, some days, I wonder if its not just Halloween everyday. I don't even care what they calles me. Jeesh, they could even call me ASSHOLE, like we calls mosts of da nurses in da areas... :wink: :idea: :!: :arrow: hahahahaahaha!! ACE

"emtgirl630", Aww, you named your puppy after me, thats sweet :oops: , now just be sure to be "kind to him" :wink: lol!! Thanks, ACE

Hi All, I would like to share my method to documentation. I didn't learn to do this properly until I had been in EMS for awhile and I wished that I had learned this alot quicker. DISCLAIMER: THIS METHOD IS ONE WHICH I USE YOUR MILAGE MAY VARY. Ok, this method as I will describe it is a modified version of the Simplified EMS Method/story method. This method is abit tedious, but alas I submit for your consideration that DOCUMENTATION is a VITAL/CRITICAL area of patient care and can vastly effect you and your patient. Don't be afraid to write an extensive, thorough, conscientious report!!!! 8) I was taught this by a conscientious Medic whose wife was a medical litigation attorney and have modified it abit to fit my own uses/prejudices/work best for me. Which I am sure that you will do as well. A major principle of this method is that "ANYONE" reading your report should have an idea of who, what, when where, why, etc.., and how the call, scene, patient, CC, etc.. presented to you and why you made the treatment/transport decisions, etc.... 1.) Dispatched to, and why, units responding. 2.) How the scene patient presents/found/ info provided to you by others (i.e.: bystander, other providers, pd, dispatch, etc...) 3.) Age, Sex, (if appropriate Race) 4.) If not otherwise listed PCP or RX MD 5.) Chief complaint, objective/subjective, etc.. 6.) Assessment, head to toe, with all +@- findings. Be sure to show that you "considered, and Ruled out" all Life Threats/Major medical disorders. 7.) Vitals 8.) known Meds/allergies. 9.) EMS Treatments and pre/post assessment-responses to it if any. 10.) Changes during TX/acuity/other levels of providers involved in care 11.) Rendering of care and report and to whom. So here is a quick basic overview of a very thorough way to document a run form. Hope this helps. Ace

Hi All, I have no idea what the address is or if it's possible but once again I ask the MODERATOR/OWNER to please post a link or repost the verysame discussion we had on the old board before switching here as it has some great info on this subject!!!!! For everyone that is interested and would like to learn the "proper RSI principles/phys, and Airway Management techniques" I would recommend you read the following items. 1.) The old posts if ever resurrected by the Owner/moderator. 2.) Walls: Emergency Airway Managemant. 3.) Mosby's Respiratory Physiology. 4.) Some of the studies I posted in the 60% Esophageal Entubation thread on this board. out here, Ace844

can the moderator please bring back a link or copy of the discussion we had about this on the old board (just before we switched to this one) where this was discussed in detail as it has some good info in it from Rid, WPM, and USAF. Thanks, Ace844

can the moderator please bring back a link or copy of the discussion we had about this on the old board (just before we switched to this one) where this was discussed in detail as it has some good info in it from Rid, WPM, and USAF. Thanks, Ace844

Hi All, You may want to consider talking to th ER/neuro docs in your area. Alot of the major hospitals in the NE are doing intra-arterial, isolated vessel TPA in angio. Meaning in short that the Neuro MD and the interventional radiologist take the patient to angiography (some cases MRA) and thread a cath via the neck to the basalar arteries. They inject the Dye, isolate the clot and thread a cath to that vessel, then release small amounts of TPA to "alleviate" the clot. This therepy has expanded the "CVA thrombolysis/lytic" window up to 6-8 hrs post sx onset. I respecfully submit it may be beneficial to yuo and your patients to find where/when/if they are doing this in your practice area. Ace

You know, this a very useful tool and in IMHLO a welcome addition to our EMS treatment toolbox. It is an out standing adjunct both in conjunction with SPo2, and ET CO2, which as previously mentioned by both Richmond and USAF, with very useful basic info. from both of them on uses, etc... the ET part of ETCO2 doesn't necessarily mean "Endo-tracheal" only. So first bit I think would be is for those who will be using them to get educated on the what/how/when/limits, etc... of the equipment/tools with which we use. In short EDUCATE YOURSELF, ASK ?'s, READ, REPEAT THE PRECEEDING 3, KNOW YOUR LIMITS AND THE LIMITS OF WHAT YOU KNOW AND USE!!!! Out here, Ace

I personally have become quite fond using either Fentanyl, or Etomidate in my Clinical practice.