DartmouthDave

Hello UGLyEMT, Airway management and rapid transport is an excellent plan. His VS could reflect hypovolemic shock. However, this fellow has cardiogenic shock or pump failure. His volume may be normal or elevated but the heart can not 'pump' it effectively. If he was more stable NTG SL or IV would help the heart pump more easily increasing vasodilation. Or, in some case, after careful assessment, Lasix to reduce the volume the heart needs to pump. However, this fellow needs something to help his heart pump more effectively. For example, as suggested by Mobey and Herbie1 Dopamine may be an options. These types of patients are very difficult to manage in any setting; hospital or in the field. Cheers....

Hello, Solid plan. RSI is what the ALS crew did for this patient. Also, CPAP was not an option. Ketamine and a cardiac patient? I have heard pros and cons from numerous people on its use on patients with CAD. According to Up-To-Date: Ketamine appears to have beneficial effects on stunned myocardium in vitro [53]. When used prior to myocardial oxygen deprivation, ketamine resulted in better recovery after reperfusion. Contractility may also improve with ketamine use [52]. Clinicians must weigh ketamine's potential cardiovascular benefits against its potential to induce cardiac ischemia in patients with significant coronary disease. Ok...the patient is intubated and copious amounts of frothy secretions are in the ET tube. The patient is hard to ventilate. Pressure is even softer and the patient is cool and toxic looking. The loading dose of Amiodarone has settled the VT issue. VS are as follows: BP 60/p HR 110 Sinus Tachycardia SpO2 90% So, the next issue is what to do about the pressure? Fluid or Pressor? Cheers

Hello, The fellow is look quite sick. His SpO2 is falling and he is becoming confused and agitated. Also, the monitor shows are run of VT that is converted by his ICD back to sinus tachycardia. GCS 13/15 (E4 V4 M5) BP 92/60 SpO2 84% Rate 30's with assessory muscle use Lungs course+++ Coughing up frothy secretions. Jeepluv77: He went in for a day procedure and had procedural sedation with Fentanyl and Diprivan. He was recovered for a couple of hours and sent home. Chrissym6: His pacemaker is set to pace a slow rate and to defib lethal arrhythmias such as VT and VF. The wife was he has had no issues with the pacemaker. Also, he was NPO since the night before for the scope. He just got home from the hospital and started to feel weak very quickly and SOB. 4C6 and other who have asked: No evidence of a lower GI bleed seen on the scope or bloody stool since. Nor any c/o abd pain. The patient has had chronic low hgb and the scope was an investigation by the pt GP. Cheers.... Nice work...

Hello, The BGL is in mmol/dl so the blood sugar is elevated. Sorry, I forgot to include the units. Herbie1 don't run away from the cardiomyopathy (CM) call. You hit the nail on the head so to speak. So, what type of CM dose this fellow have? His wife said his heart was 'big' and 'floppy'. Also, what is in importance of the 'zap' he felt on the way home? The patient nor his wife had had this happen before. Lastly, a slight omission, I forgot to add that he was on PO Amiodarone. Sorry. Lots of distractions these days. I will do a follow up post here in a little while more vitals and information. Need to go for a coffee run..... Cheers

Hello, Sorry for the slow response. Got tied up at work. The wife can not find the pacemaker information card. She says it is for when his heart beats too fast it zaps him and speeds things up when his heart is too slow. It was inserted after his MI because his heart got 'too big' and would 'go to fast' and the patient would 'pass out'. The Dr told the husband and wife that his scopy was normal for his agen and no bleeding was noted. He was given so 'white stuff' and some pain medications. He recovered quicky and was discharge home. The wife also add that Walter felt a funny 'zap' in his chest on the way home. Since then his troubles have started. His medications are: ->Ferrous Sulfate/Levothyroxine/Glyburide/Atrovastin/Sprilactone/Lasix/Ramipril/Metoprolol Your partner inserts an IV and connects the patient to your monitor while you conduct a more detailed physical exam. The physical assessment notes: ->course crackles BL ->no edema ->skin: cool and diaphoretic ->BGL:12.6 ->EKG: Sinus Tachycardia @ 120-130 Cheers... Have to run.....

Hello, ALS is requested by a BLS crew that is on scene. You arrive to a nice suburban home and proceed inside. You are greeted by one of the responding PCP. She briefs you about the situation. Walter, a 72 year-old male had his wife call for an ambulance for worsening SOB and fatigue. Walter has a history COPD, NIDDM, CHF, AMI (8 years ago), numerous episodes of VT and had a ICD and Pacemaker inserted as well. He has just came back from the hospital were he had a colonoscopy done as an investigation for a low Hgb. No active bleeding was found during the scope. He has been NPO since yesterday. He also hasn't taken any of his medications since yesterday as advised by the endoscopy clinic. Walter is sitting in his living room. He appears frail. He is working hard at breathing and has a wet cough. His skin is diaphoretic and pale. VS as per the BLS crew: GCS 15/15 BP 120/60 HR 120 Rate 38 SpOs 88% on 15 lpm Cheers...

Hello, The case that I interject with was a interesting mixed-OD that came through the hospital. There was one thing I wanted to ask poison control when they called. Our patient had chronic pain issues and required a fair bit of sedation to ventilated on A/C. Now, what I was wonder was this, "Could we use Propofol infusion for sedation?" Propofol has a high lipid content. An infusion at 200mg/hr is 20cc/hr or 480cc of lipids (plus boluses prn) a day, for example. I know this is sort of crazy idea. Just wondering......... I have hit various data bases and I have not been able to find an answer. Nor, do I have the 'nads' to call up poison control and ask them. They are too busy. Cheers

Hello, Sorry, the insulin therapy was started in the hospital. EMS used the standard Glucagon and the CaCl. All in all, things worked out well for this fellow despite a massive OD and numerous brady arrests. Cheers

Hello, A hard situation because most of the drugs you needed are not available or you won't have enough on hand. However, an other consideration could be Dopamine for services that carry it. Had a mix OD at work recently. One of the medication he OD on was Diltiazem SR tablets. The standard CaCl infusion wasn't helping. So, Poison Control suggested 'High Dose Insulin Therapy' and 'Lipid Therapy'. Crazy stuff. In effect, you run an insulin infusion an 1-2 units/kg/hr (this fellow was at 250 units/hr) along with a D20W or a D50W infusion (to prevent hypoglycemia....a 1000cc bag of D50W is the oddest looking thing!!). Somehow, the insulin blocks the CCB cardiotoxic effects. Plus, the insulin/glucose increase cardiac output as well in a similar fashion to the 'stress response'. The lipids (basically TPN solution) binds with the CCB as well. I thought I would throw this out there because it was so unique and interesting. Cheers

Hello, I wouldn't sedate the patient or use Cogentin for the trmors. Also, it is my understanding that Cogentin is mainly used for EPS effects (parkinsonian symptoms, dystonia, akathisia and tardive dyskinesia) of medications. I am not sure if it would help with this patient's tremors. However, I am far from an expert on Cogentin. I degress..... Will the 12-lead/3-lead change the care you provide? In most cases...no. If you can offer pre-hospital thrombolytics and you have a long transport time their could be some use to giving Ativan (ect...) to get a 12-lead to see if their are ST-elevations. If you have a short run to the hospital I wouldn't sedate. If you only have the standard M.O.N.A. treatment options sedation for a 12-lead won't change what you are going to do too much. IMHO. Cheers

Hello, Here is a related story from the NWT in which a psy patient jumped from the medevac plane (fixed wing): Fatal Jump Cheers

Hello, From my understand and research on this topic (for what it is worth) TSS is a DDX of SJS. The rash from TSS is described as 'red lobser-like' in appearance. Whereas, with SJS/TEN the lesion rupture. Pre-hospital care, in general, for TEN, SJS, and TEN is supportive in nature. We had a TSS here in our ICU ago a year ago. She was one of the sickest people I have seem in awhile. We knew she was septic but the cause was a mystery until an nurse note a tampon during a bath. This was on day 3 of her admission!! Cheers

Hello, Since the cat is out of the bag I guess we can discuss some of the finer points of management of this syndome. According to Up to Date: Stevens-Johnson syndrome — SJS is the less severe condition, in which skin sloughing is limited to less than 10 percent of the body surface [1]. It is characterized by a prodrome of malaise and fever, followed by the rapid onset of erythematous or purpuric macules and plaques [1,2]. The skin lesions progress to epidermal necrosis and sloughing (picture 1A-. Mucosal membranes are affected in 92 to 100 percent of patients, usually at two or more distinct sites (ocular, oral, and genital) [3]. Whereas, Toxic epidermal necrolysis — Toxic epidermal necrolysis (TEN), or Lyell's syndrome, involves sloughing of greater than 30 percent of the body surface area [1]. TEN also begins with a prodrome of fever and malaise, although temperatures are typically higher than those seen with SJS, often exceeding 39 degrees Celsius. Mucous membranes are involved in nearly all cases [4]. The skin lesions are widely distributed erythematous macules and patches, although about 50 percent of cases begin with diffuse erythema [1,5,6]. In the early stages, skin pain may be prominent and out of proportion to clinical findings [7]. The skin lesions progress to full-thickness epidermal necrosis leads. The ultimate appearance of the skin has been likened to that of extensive thermal injury (picture 2A- [5]. In effect, TEN is repersents worsening SJS. Also, as noted by CM (if I recall correctly) SJS/TEN can effect various body systems. In this case, the patient's lungs are effected. See below: •Pulmonary - Pulmonary complications of TEN may include dyspnea, hypoxia, bronchial hypersecretion, tracheobronchitis, pulmonary edema, bacterial pneumonitis, and bronchiolitis obliterans [41,42] (a.k.a. B.O.O.P) This fellow is barley holding his own. He is tired and in a great deal of pain. The lesions cover about 20-30% of his body. Resp are in the 30's and his SpO2 is 86% and refractory to high flow O2 (creeps up to 87-88%). There are course crackes all lobes and the patient is having a great deal of trouble with his inspiratory phase (having trouble expanding his lungs). His VS are as follows: GCS 15/15 Anxious BP 180/100 HR 130 SpO2 87% on 15 lpm IVx2 is started.

Hello, Nice. Yes, he has SJS. Good show. I have heard about it. But, I have never seen it until last week when a fellow came in to the ED with it. I figured it would be a good case study. I have never heard about Manute Bol. But, I Googled it and it seems he was a NBA player that died of SJS. I don't follow the NBA at all. LOL! I thought I was clever....guess not! =) So, now what? =) Cheers...

Hello, You are an ALS crew in a city of 300,000. There is a large teaching hospital and two smaller community hospitals. You are dispatched for a 58 year-old male with a complaint of a boils and SOB. Once on scene your are greeted by the patient`s wife. She is quite anxious but holding things together. Her husband did not want an ambulance called be she vetoed him. She says he has a horrible rash on his face, arms and inside his mouth. It started three days ago and has been getting worse. Much worse. He also has had trouble breathing and has cough up some bright red blood for the past four hours. She usher you into an upstairs bedroom. The patient is sitting in bed with three large pillows behind his back. He looks tired and quite toxic. He has no shirt on and his face, upper chest, and lips and tongue are covered red lesions of which quite a few have the skin sloughing off. His face looks puffy as well. His wife said that he had pneumonia and a sore throat a two week ago and was Zythromax and also started some medication for gout. Other than she has been very healthy. Cheers....

Hello, I would say unstable due to a low BP, very low Hgb, and an obliterated white count. With such a low white count I think reverse isolation may be a good idea. Plus, isolation gowns for staff as well. With such a low BP she need her tank filled with NSS and PRBC until her CVP is elevated. Then if need be a pressor. This is a viral illness. I am not sure if an anti-viral (Acyclovir?) may be benifical or not. I have never seen DHF myself. Prognosis. Not too bad. I have seen some really bad septic patients walk out of the hospital with good care. Cheers PS....I appears that I was typing this when your were doing an update. LOL!

Hello, Well, if we are in the ED I figure we would start with the Sepsis of unknown source protocol (whatever the abx may be for this) plus blood cultures, urine cultures and sptum cultures. Plus, lytes, LFT, coags, and BUN/Cr. If there ID consult them as well. Get a CXR, ABG an arterial line and central line (once coags are check). More fluid as well. As for the cause, I need to dig on this some. Dengur fever (DHF) maybe. Just a mad guess. Cheers

Hello, I can not think of adding anything in reference to the NSTEMI. It has been covered quite well by the previous posters. I suspose, that the normal standard of care for a NSTMI is an angiogram at some other point. From what you have written about the 'partial quadriplegic'(poor arm ROM and sensation changes)and the MOI (playing hockey)it sounds like a 'incomplete' or 'partial' cord injury. The spinal corad in fact is made up of numerous tracts. One for motor control. One for pain. One for deep sesation (i.e. the pressure one feels on their feet when standing). There are many types of partial cord injuries. This one sounds like Cental Cord Syndrome (CCS). I have added a couple of wik links about the various cord syndromes. CCS ACS (Anterior Cord Syndrome) Brown-Sequard Syndrome Best of luck to you and your family. Cheers... PS....Pardon any typo. I am firing this off while at work.

Hello, Funny and offensive all at the same time. Let the bashing begin! Cheers

Hello, If you are worried about cash just use any of the NCLEX study guides. They go over how the test is laid out and the questions are structured. Also, there are practice test in the book and a CD that you can do a dry run exam. That is all I did. It worked out well for me. Considering I did go to school in the US and their were a few difference that I had to get my head wrapped around. I used the Keplan textbook. Save the money for a prep-class. IMHO all they are going to do is teach you the study guide. Best of luck.... David

Hello, Here is a decent link about ASA OD: ASA OD There were two goals I had with this case study. 1. ASA and glucose 2. Airway Management First, there is an interesting tidbit glucose utilization. ASA in toxic levels can inhibit utilization of glucose within the CNS despite a normal serum glucose level. So, an altered LOC with a suspected should get some glucose in most cases. "Increased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, although the serum glucose levels may sometimes be within the normal range. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose and symptoms of CNS hypoglycemia (eg, altered mental status) may occur even when blood glucose levels are within the reference range." I based this case study on a fellow that came into the ED and then the ICU. He was given an amp of D50W and D5W with NaHCO3 was started. Second, airway management. Most sources (Up to Date, ect...) stated that intubation of an ASA OD should be avoided. ASA OD causes central nervous system hyperventilation. Which cause a profound resp. alkalosis. This helps prevent binging of H+ to the Sal- to for HS (acid). Anything that disrupts this can cause a rise in HS (acid) in the blood. They only time intubation is warranted if if their is depressants on board. Which is the case in the scenario. Really, a good argument can be made for intubation as well as avoiding it. Cheers Hello, I am sorry to say I am very weak on ETCO2 waveforms. What I can say is the ETCO2 is correct. Here is the thing with the CO2. An ASA OD causes central nervous system hyperventilation. Thereby causing a resp alkalosis. At the same time an ASA OD will cause a medabolic acidosis (low HCO-). An ABG would show a mixed resp alkalosis and a medabolic acidosis. Without the hyperventilation the acidosis would be much worse! The ETOH and MSIR is bad news here. It lowers the resp rate and volume. Thereby, taking away the compensation caused by the hyperventilation. This is why the Narcan was a good idea. Plus, the NaHCO3- for the acidosis (worsen by the hyopventilation). A low CO2 is a good thing here. Cheers

Hello, First, I think it is safe to say this lady is septic because of the history and the fact that she meets two of the Sepsis/SIRS criteria. A HR above 100 and a resp rate of 20. Now, a temperature would be nice. If not, is the skin hot? Cool? Also, her BP is low. More importantly, her DBP is only 40. As for the cause. Not sure. The petechia and the blood shot eyes are worrying. As for treatment. Lets get this lady in to the ambulance. Start an IV, a 500cc bolus to start. Do an EKG and get her in to a hospital gown. See anything new? Any photophobia? Stiff neck? Pain when she flexes her legs? Travel immunizations? N+V? Diarrhea? Cheers

Hello, His ETCO2 is 19mmHg. Also, I think that an amp of NaHCO3 is a reasonable plan. He is loaded up in the ambulance and you are getting geared up to go to the hospital.

Hello, I would start by assessing the patient while my partner gets some vital signs (including a temp). What is this lady's general appearance? Skin colour? Jaundice? Frail? What is her enicity? Recent travel? Cheers

Hello, Sorry for the slow response. Very busy at work these days. Excellent responses here. The Wife: She is quite drunk. She is unable to offer any medical history. However, she says he was unable to talk right. Had all his words mixed up and was more violent and disagreeable than usual. It reminded her of her Grandmother when her sugars were low. RCMP: Police MSIR: Morphine Sulfate Immediate Release Tabs Gabapentin: An anticonvulsant that is commonly used now for carious chronic pain syndromes. ASA: As noted above Aspirin. So, it appears that he has taken quite a few Morphine pills and a pile of ASA. The bottle had 50 325mg tabs in it! They are all gone. Plus, washed it all done with liberal applications of ETOH. Some excellent suggestions of treatment. IV x2 and a bolus is started. OK, he is given some Narcan for the MSIR OD. With careful titration his wakes up some. He is reassesses and the following findings are noted: GCS 11/15 (E4 V2 M5) His eyes are open and he is trying to talk but his speech is all mixed up. He has a confused but mean look in his eyes. His arm and legs are quite weak and shaking slightly. PEARL @ 3mm Skin: Diaphoretic BP: 120/60 HR: 90's NSR Resp: 36 Very rapid and deep. His mouth is dry as a bone. His lungs are clear. BGL: 7.5mol (135 mg/dl) What is our field dx here? Second, what impact would this have on airway issues? Cheers...