Just Plain Ruff

I think anytime that a hospital is revealed to have higher than industry norms in death rates. length of stays, and other items they become beter at that specific thing. You've all heard of the 30 minute or less guarantee - that was directly a result of the focusing on the waiting times for patients in the ER's. No hospital wants the spotlight shined on them. Things get changed when admin's get their faces shined on.

In your opinion, what would constitute acceptable risk in this case? well this was an acceptable risk to me. As long as after you determined it might be poisoning and need of decon you already have been exposed to a significant degree. Just take the guys clothes off and wash him off if you can. You already have pt. contact so you cant' run away with the excuse - oh he's contaminated we cant treat him until he's decon'ed, you are already exposed. Just deal with it the best you can. What would be your deciding factors in risking the decontamination process yourselves? The guys gonna code if you don't do anything - you are already contaminated - see above. Do you feel adequately trained and equipped to manage a specific case like the one that has been presented? Absolutely Would you even attempt it regardless of the patients condition and wait time? Yes I'd take all his clothes off , turn the hose on and wash him off in the house. Then move my butt and get him to the ER. There certainly comes a time when your safety and that of your partner becomes priority? Is this one of those times? I feel relatively comfortable in this type of situation as long as I know the risks and issues. I would definately contact the hospital and let them know what i had. But unfortunately I'm already exposed and as long as I limit my exposure by removing the toxin from the area and the patient then I relatively feel safe in continuing to treat this patient. I would probably call for a 2nd unit anyway so they could meet up with us or follow us in in case me and my partner start to have symptoms. I'm giong to be very cognizent of how I feel as well as how my partner feels. I'd expect a full workup by the ER on myself and my partner if we even remotely started to exhibit any symptoms.

the cause of your issue is the old owners. Letting her play by growling and nipping. If you consistently correct your dog and I mean consistently you can break her of the behaviour. It is senseless to put this puppy down just because the old owners were doofus's and let her bite and growl when playing. Just continue to correct her and she will begin to learn but I second what Lone said, correcting a behaviour that is in her genetics and nature is going to be difficult. The other thing I urge you to do is to limit the behaviour and activity that is bringing out the worst in the puppy. Ergo. letting the dog play with the kids without supervision. someone of authority needs to be watching the dog and correcting the behaviour when it happens rather than correct it afterwards. If the dog is immediately corrected then the behaviour will cease quicker. ONE NOTE - DO NOT punish the dog for something it did earlier in the day. The dog has no idea what it did and all it understands is that you the owner is beating it for no reason.

Isn't working as a paid paramedic for a volunteer service an oxymoron/?

I'm gonna RSI the guy if I can but if not I'll try to nasally intubate him if he tolerates it but I'm betting he won't. this guys gonna code shortly. This is a no-win situation. did we give the 2pam and atropine?

I agree Cb I'd have worked him even without my service requirements.

ok this guy fell from 24 feet he landed directly on a cinder block dead(no pun intended) in the chest he suffered a traumatic rupture of the aorta a traumatic rupture of the esophagus and a tramatic tear in the trachea after multiple views of the trachea and looking at the tube going thru the vocal cords not until autopsy did we realized the damage to this guys internal setup. The reason why the belly kept getting bigger was that the air was going in the lungs (hence the appropriate readings of the etco2) and it was going into the belly thru the tears. This guy was dead when he hit the ground but our service required all traumatic arrests with any type of rhythm to be worked.

You do not have a ng tube to drop

Terri you are close. Keep digging and you will come up with the answer This was a actual call I ran a number of years ago.

Air does go into the chest via auscultation. ETCO2 is very good Abdomen is still rising albeit not so fast now.

Ok, apparantly this guy fell from a tree approximately 24 feet off the ground landing on the cinder block. With ventillations chest goes up and down as does the abdomen. You intubate him and two large bore IV's goin. You have 15 minutes to the ER. ETCO2 is good with intubation But you notice that the abdomen is getting bigger and bigger with each successive ventillation. What needs to happen.

Neither

your service requires you to work all trauma codes regardless of whether you think they are viable or not. this is based on the new trauma center that just opened in the city limits which allows for you to have a transport time of less than 15 minutes at any time but... the caveat here is that the trauma center has to be open and not closed and today - it's open.

He was out in the back, the wife doesn't know what he was doing out there but he did say something about trimming the trees. Wife says no allergies, only med is a cholesterol med with subsequent history of Hyperlipidemia It is 74 degrees outside Obvious injuries - well he's on top of a cinderblock You control c-spine and roll him off the block and you open his shirt and you see a cinderblock like impression on his chest and upper abomen He is not breathing, does not have a pulse, your protocols are to work trauma codes regardless of whether you feel that he is viable or not. Air goes in very nicely when ventillating him but both chest rise and abodomen is noted to rise. EKG Shows wide complexes at 34 per minute What now?

Classic story from Australia. SYDNEY, Australia — The president of a male-heavy mining town in Australia Called created uproar among local women over the weekend by inviting "beauty-disadvantaged" women to join the population of lonely men. Mayor John Molony found himself under attack Monday over comments he made to a local newspaper that read: "May I suggest if there are five blokes to every girl, we should find out where there are beauty-disadvantaged women and ask them to proceed to Mount Isa." The mayor added that many women who already live in the remote Queensland state town seem quite happy. "Quite often you will see walking down the street a lass who is not so attractive with a wide smile on her face," he continued. "Whether it is recollection of something previous or anticipation for the next evening, there is a degree of happiness." The quotes, published Saturday in the Townsville Bulletin, sparked outrage among the town's female population, led to furious online debates and drew criticism from the local chamber of commerce. "There's a lot of anger circulating among the community at the moment — a lot of passionate anger," Mount Isa Chamber of Commerce manager Patricia O'Callaghan said Monday. "There's a lot of women voicing their opinions." Molony declined to elaborate on his comments Monday except to say they were "twisted and warped" by the newspaper. "I've been shredded," he added, before hanging up the phone. The situation may not be quite as dire as Molony noted. According to the 2006 census, males made up 52.6 percent of the town's population of nearly 20,000. Local women, enraged by the mayor's comments, protested Monday, saying there aren't a lot of gems to be found among Mount Isa's men, either. "We want an apology," local woman told the Brisbane Times.

Get a call for a man who is found on a cinder block. If you all know what a cinder block is - it's the 2 foot by 1 foot block of concrete with two square holes in it. It looks like a domino but made of concrete. Wife just walked out from the house to the backyard after not hearing from him for about 30 mins. He has no pulse and is not breathing. What do you want to know?

cost of this game? I'd be interested in playing this but what will be the monthly fee be to play this game?

Here is what happened to the baby in the ER after you dropped off the baby into the arms of the new pediatric resident Upon physical examination, he was dusky and floppy and had a temperature of 36.3° C, a heart rate of 170, a respiratory rate of 45, and a blood pressure of 64/45. He had not received any paralytic agents. His oxygen saturation levels were unobtainable. A subconjunctival hemorrhage was noted in the left eye, and his fontanelle was soft and flat. There were coarse breath sounds bilaterally, and his heart had a regular rhythm with no obvious murmur. His abdomen was firm and full, without bowel sounds. His liver edge was not palpable given his firm abdomen. His extremities were cool with thready pulses and a delayed capillary refill time of 5 to 6 seconds. In the ED, umbilical lines were placed for intravenous access, laboratory tests were made, and the baby was given doses of ampicillin and cefotaxime (50 mg/kg of each). Initial laboratory evaluation demonstrated a pH of 6.73, base deficit of -30 mmol/L, glucose of 175 mg/dL, sodium of 133 mmol/L, potassium of 7.5 mmol/L, and hemoglobin of 14.2 gm/dL. Additional laboratory tests included a complete metabolic panel, lactate, ammonia, and blood and urine cultures. He was given a saline bolus of 10 mL/kg and sodium bicarbonate for hyperkalemia and his base deficit. A chest x-ray showed cardiomegaly (Figure 1). The patient's ammonia level was elevated at 578 micromole per liter (mcmol/L) with a lactate level of 24.5 mmol/L. Blood urea nitrogen level was 24 mg/dL with an elevated creatine level of 2.2 mg/dL. Return to Journal CME Table of Contents -------------------------------------------------------------------------------- Printer-Friendly Email This In This Article Introduction -------------------------------------------------------------------------------- References From Medscape Emergency Medicine Cases in Pediatric Emergency Medicine A Newborn Presenting in Extremis CME/CE Posted 01/25/2008 Christy A. Meade, MD; Ghazala Q. Sharieff, MD Disclosures Introduction Managing a toxic, decompensating newborn can be a stressful and difficult task. There are significant physiologic changes associated with birth, and multiple congenital abnormalities that can present shortly thereafter. The differential diagnosis can be immense and overwhelming. The mnemonic THE MISFITS can aid in the vast differential diagnosis (Table 1). This case discusses a 5-day-old who was brought to the emergency department (ED) with the chief complaint of difficulty breathing. Table 1. THE MISFITS. Causes of Shock/Severe Illness in the Newborn T Trauma/nonaccidental trauma (NAT) H Heart disease - congenital E Electrolyte disturbances M Metabolic disturbances (congenital adrenal hyperplasia) I Inborn errors of metabolism S Sepsis F Formula dilution or over concentration I Intestinal catastrophes T Toxins (home remedies) S Seizures/central nervous system (CNS) abnormalities Case Report A 5 day-old-male is brought to the ED with tachypnea and increasingly labored breathing. He was born at full term and had no difficulties after birth. Prenatal care and ultrasound were unremarkable. He was with his parents in Mexico when they noticed that he did not awaken for his 6 AM feeding and that he had slept for 7 to 8 hours in the afternoon without urinating (no wet diapers during that time period). At about 8 PM, the parents noted that he was laboring to breathe by breathing rapidly and making gasping noises. The baby was taken to the closest Mexican clinic, where he was found to have an undetectable blood glucose level and to be in respiratory distress. An intravenous line was inserted, bolus doses of dextrose 10% in water were given, and he was intubated. He was then transported across the border to the closest US children's hospital. Upon physical examination, he was dusky and floppy and had a temperature of 36.3° C, a heart rate of 170, a respiratory rate of 45, and a blood pressure of 64/45. He had not received any paralytic agents. His oxygen saturation levels were unobtainable. A subconjunctival hemorrhage was noted in the left eye, and his fontanelle was soft and flat. There were coarse breath sounds bilaterally, and his heart had a regular rhythm with no obvious murmur. His abdomen was firm and full, without bowel sounds. His liver edge was not palpable given his firm abdomen. His extremities were cool with thready pulses and a delayed capillary refill time of 5 to 6 seconds. In the ED, umbilical lines were placed for intravenous access, laboratory tests were made, and the baby was given doses of ampicillin and cefotaxime (50 mg/kg of each). Initial laboratory evaluation demonstrated a pH of 6.73, base deficit of -30 mmol/L, glucose of 175 mg/dL, sodium of 133 mmol/L, potassium of 7.5 mmol/L, and hemoglobin of 14.2 gm/dL. Additional laboratory tests included a complete metabolic panel, lactate, ammonia, and blood and urine cultures. He was given a saline bolus of 10 mL/kg and sodium bicarbonate for hyperkalemia and his base deficit. A chest x-ray showed cardiomegaly (Figure 1). The patient's ammonia level was elevated at 578 micromole per liter (mcmol/L) with a lactate level of 24.5 mmol/L. Blood urea nitrogen level was 24 mg/dL with an elevated creatine level of 2.2 mg/dL. Figure 1. Chest x-ray showing cardiomegaly. Given his decompensated state, with cardiomegaly and elevated ammonia level, ED staff called for cardiology and genetics consultation. Repeat arterial blood gas prior to transfer to the newborn intensive care unit (NICU) showed a pH of 7.16 with a base deficit of -19 mmol/L. An echocardiogram was performed upon arrival to the NICU that was consistent with hypoplastic left heart syndrome with aortic and mitral atresia. The ascending and transverse aorta were severely hypoplastic and there was severely reduced right ventricular function. An atrial septal defect was present with left to right flow and there was a moderate patent ductus arteriosis. The patient was started on prostaglandin E1 (PGE1) and dopamine for inotropic support, and the cardiothoracic surgery department was consulted. Further discussion The differential diagnosis of a decompensating newborn can be extensive and includes infectious causes, hypoglycemia or electrolyte disturbances, metabolic disorders, congenital adrenal hyperplasia, renal failure, hematologic disorders, gastrointestinal disorders, neurologic disease, and trauma. A few common tests may narrow the differential diagnosis, including glucose, electrolytes, complete blood count, ammonia, lactate, and chest and abdominal x-rays. This patient's major findings in the ED included hypoglycemia, acidosis, hyperammonemia, and cardiomegaly. These findings trigger concerns for cardiac or metabolic disease. However, there is always a concern for sepsis in a toxic newborn, and antibiotics should be given promptly. Hypoglycemia in an infant is usually transient and secondary to hyperinsulinism or glycogen depletion. More persistent hypoglycemia can be derived from more significant illnesses, including congenital adrenal hyperplasia, growth hormone deficiency, panhypopituitarism, congenital hyperinsulinism, inborn errors of metabolism, hepatic disease, and sepsis. Hypoglycemia in a newborn should be treated with dextrose (0.1-0.2 g/kg/dose or 1-2 mL/kg/dose of 10% dextrose solution) immediately and if needed, a continuous infusion can be started (4-6 mg/kg/minute). Hyperammonemia is the hallmark of an inborn error of the urea cycle. The most common presentation is a 2- to 5-day-old male who has poor feeding, emesis, and decreased mental status. Males are primarily affected by the X-linked disorder ornithine transcarbamylase deficiency. Although our patient did have an elevated ammonia level, acidosis from any cause results in a nonspecific downregulation of the urea cycle, which results in hyperammonemia. Cardiac malformations account for approximately 10% of infant mortality and almost all pediatric cardiac-related deaths. The incidence of congenital heart disease is 8 to 10 per 1000 live births. The most common lethal heart defect in the neonatal period is hypoplastic left heart syndrome. This patient did have cardiomegaly with acidosis, which led to the concern for heart disease. At birth, there is a transition from right-sided fetal circulation to left-sided circulation. The decrease in pulmonary vascular resistance results in closure of the ductus arteriosus, ductus venosus, and foramen ovale. Depending on their cardiac defect, infants may be in extremis with cyanosis, have respiratory failure, or be in shock. Left ventricular outflow tract obstructions are the most common subset of ductal-dependent lesions and include hypoplastic left heart syndrome, interrupted aortic arch, coarctation of the aorta, and aortic valve stenosis. Left ventricular outflow tract obstructions account for 12.4% of cases of congenital heart disease in infancy. Hypoplastic left heart syndrome (HLHS) is a combination of mitral valve atresia, severe aortic valve stenosis, a hypoplastic left ventricle, a hypoplastic ascending aorta, a patent ductus arteriosus, and a patent foramen ovale. When pulmonary vascular resistance decreases after birth, the obstruction of the left ventricular outflow results in a higher percentage of fixed right ventricular output to the lungs instead of to the body. Although increased pulmonary blood flow results in higher oxygen saturation, systemic blood flow is decreased. Perfusion becomes poor and metabolic acidosis and oliguria develop. Coronary artery and cerebral perfusion also are dependent on systemic blood flow through the ductus arteriosus. Therefore, increased pulmonary blood flow results in decreased flow to the coronary arteries and brain, with a risk for myocardial or cerebral ischemia. PGE1 should be started as soon as possible at 0.05 to 0.1 mcg/kg/minute if ductal dependant congenital heart disease is suspected. These patients should be monitored closely as side effects include apnea (10%), hypotension, bradycardia, and seizures. Intubation may be necessary, especially if the patient must be transported. Patients should be transported to a center skilled in pediatric cardiac surgery. Oxygen saturations are expected to be lower (70s or 80s) and 100% oxygen should not be given. Higher oxygen saturations increase pulmonary blood flow, leading to pulmonary edema, and decrease systemic flow, resulting in acidosis. Without staged reconstructive surgery or orthotopic heart transplantation, HLHS is uniformly fatal, usually within the first 2 weeks of life. Survival for a longer period occurs rarely and only with persistence of the ductus arteriosus. Orthotopic heart transplantation results in early and long-term success similar to that of staged reconstruction. Among low-risk patients who undergo staged reconstruction or transplant, survival at 5 years is approximately 70%. Most studies report neurodevelopmental disabilities in a significant number of patients who survive either staged surgical reconstruction or cardiac transplantation. Our patient stabilized on PGE1 and underwent the first stage of reconstructive surgery. His course was complicated by 2 episodes of line sepsis and feeding difficulties. He was discharged to home after 4 weeks and is now awaiting further surgeries.

you check on all that was listed above. No injuries to anyone but the driver and he is refusing treatment. you re-check the baby and all is well You have given a 2nd bolus of fluid and the heart rate is now 160 the child seems to be a little pinker and moving a little better. You have requested 2 ambulances - one for your baby and one for the driver of the car. Your partner is now suffering his own pucker factor because he went thru the red (but followed all the rules of the company) and he is thinking of the last two guys who had this happen to them and they are still trying to find a job. You hear in the background more sirens than you can imagine ever hearing in your life. 3 fire trucks, 5 police cars, 2 ambulances and 1 supervisor along with the owner of the company arrive. You put the baby in the 1st ambulance, jump in and haul butt to the hospital leaving your poor partner to fend for himself. What now?

Did anyone question the D25 dosage given earlier? What do you want to check after being hit by the car. Is there something you want to immediately check?

Intubation was definately one of the right steps Fluid bolus given with mild results You are about 6 blocks from the hospital and your ambulance struck on the passenger door side by a driver who had the green light and you had the red. (you were running L&S though). Your ambulance is dead in the road. No injuries to you, mom or baby or partner but what happens now? Remember we have a 5 day old tubed, scalp veined and very very sick What happens now. (You didn't think I was gonna let you get to the hospital that easy did you??????)

remember you've already given glucose - You intubate this little bundle of pucker factor joy and assist his respirations - hence giving him a rest and doing the work for him. YOu also give him a 10ml/kg fluid bolus. What do you expect to see after these two procedures? You are now 5 minutes from the hospital

I don't make the scenario up, it's the docs that did this one. ha ha

well they were visiting family in the small town in mexico. come on guys, theres one treatment that no-one has suggested. the baby is gasping and his resp rate is now 10 and his heart rate is 210 now. There is one thing that will probably help this kid right NOW Glucose didn't do much. You are still 20 minutes out from the hospital.

beginning site - not much there. paramedicspace seems DRT. links to other sites like that will probably get deleted. but a nice start