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Croup/Epiglottitis

12/19/2010 by Adam Thompson, EMT-P 6 Comments
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There is nothing scarier than a sick kid.  I am becoming more and more obsessed with educating myself on pediatric emergencies.  This is because of that fear, and the fact that I find it is one of those areas that I am less versed in.  This post is aimed at identifying and treating the child who presents with an upper respiratory infection (URI) like croup or epiglottitis. These kids sound sick, look sick, and may get even sicker.

As always, aggressive airway management may be indicated if the child appears to have impending respiratory failure.  Signs of this include severe hypoxia, bradycardia, and decreasing respiratory effort.

If the patient doesn’t present with imminent signs like those mentioned above, it is pertinent to obtain a good medical history.

History:

Has the child ever had a URI in the past?

- If so, did he/she present like this?

Was the onset acute or gradual?

- Epiglottits generally presents with an acute onset.

Has the child been sick, and is he up to date with vaccinations?

- Most cases of epiglottitis are caused by haemophilus influenza or H.flu

Has the child ever been intubated?

- This helps identify whether you will need to be aggressive, and a recent intubation could be the cause of hoarseness.

Epiglittits is actually inflammation of the epiglottis–you know, that flap that covers the trachea during swallowing?  If this becomes inflamed, it swells, and that swelling could cause a partial or even a complete occlusion of the trachea, thus compromising ventilation.

- Usually febrile, without cough

- Patient may be in tripod position

- Drooling present

Treatment

- Immediate intubation may be indicated (may be very difficult!)

- Epinephrine may be administered in extremis

Croup or laryngotracheobronchitis is also an upper respiratory infection that may be mild, moderate, or severe.  It tends to be worse at night, and is most commonly identified by the classic “seal-bark cough”.

- Inspiratory stridor & “barking cough”

- Often preceded by flu

- More likely if they have had croup before

Treatment

- Oxygen therapy

- Nebulized Saline

- If severely hypoxic, racemic epinephrine may be indicated.

- It is often taught to take these children outside, into colder air

So who is in extremis?

- The severely hypoxic child: Cyanosis, bradycardia

- Intercostal retractions with decreasing stridor is an ominous sign of impending respiratory failure

- Decreasing mental status means decreasing respiratory drive.  TREAT AGGRESSIVELY

****

Check out Justin, The Happy Medic, Schorr’s last run-in with croup in THIS POST.

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Filed Under: Airway, Airway Management, Education, Medical Emergencies, Pediatrics

Differential Diagnosis Series – Abdominal Pain (Part 2)

09/15/2010 by 510medic 2 Comments
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This post is the second of two detailing the construction of a differential diagnosis for abdominal pain.  The post yesterday consisted of a review of the relevant history and physical exam for abdominal pain patients.  This article is also posted at my site:  510medic.com

COMMON EMS DIAGNOSES
While many causes for abdominal pain require lab work and diagnostic studies in the hospital environment, there are some common or potentially life-threatening diagnoses that are considering “can’t miss” in the prehospital setting.

APPENDICITIS
Appendicitis, as the name might suggest, is inflammation of the appendix.  Caused by blockage of the entrance of the appendix, the organ swells, eventually bursting and filling the abdominal cavity with infectious material.  The result of an abdominal infection is peritonitis, another life threatening condition.  Traditionally, there are several signs that have been taught to EMS responders to determine if a patient has a probable appendicitis:  fever, rebound, guarding and tenderness over McBurney’s point.  As it turns out, fever is neither sensitive (15-67%), nor highly specific (85%) for appendicitis (1).  As a refresher, this sensitivity means that 15-67% of abdominal pain patients with no fever (a negative finding) will not have an appendicitis.  Needless to say, this number does not inspire a lot of confidence in ruling out appendicitis.  Conversely, 85% of patients with an appendicitis will have a fever (1).  McBurney’s point (halfway along a line drawn from the umbilicus to the iliac crest) is no better,  Tenderness over that point is present in only 50% of appendicitis patients.  Lastly, rebound has a sensitivity of 61% and a specificity of 82% and guarding has a sensitivity of 46% and a specificity of 92% (1).  So what this all means is that a patient with abdominal pain and all of the following symptoms:  fever, pain over McBurney’s point, guarding and rebound tenderness likely has an appendicitis.  What this also means is that a patient can have abdominal pain and none of the other symptoms and still have an appendicitis.

ECTOPIC PREGNANCY
An ectopic pregnancy occurs when an embryo implants somewhere other than the uterus.  Most often, this implantation occurs in the fallopian tube and can cause a rupture as the pregnancy progresses.  This obviously represents a significant threat to the life of the mother.  As ruptured ectopic is the leading cause of pregnancy-related death during the first trimester (2), it is important to keep a high index of suspicion, since a patient may not yet know she is pregnant.  To this end, any female patient of child-bearing age presenting with abdominal pain, syncope, hypotension or vaginal bleeding should be considered for a possible ruptured ectopic.  Pain from a ruptured ectopic pregnancy will typically present in the right or left lower quadrant (depending on which side the pregnancy implanted) and may present with profound hypotension.  Ultimately, clinical findings cannot effectively  rule out ectopic pregnancy and an in-hospital ultrasound is needed (2).

PANCREATITIS
Pancreatitis is inflammation of the pancreas occurring in either chronic or acute forms.  Chronic pancreatitis can result from alcohol and illicit drug abuse and, as such, is more often seen in the prehospital setting.  Most of the actual diagnostic work for pancreatitis takes place in the in-hospital setting.  Lab values are particularly helpful including pancreatic function tests and, of course, the ever-present abdominal CT (1).  In the prehospital setting, most of the leg work goes towards history-taking.  Patients with epigastric pain, often radiating to the back, with associated nausea and vomiting and a history of chronic alcohol abuse who have been ruled out for cardiac and respiratory causes should be considered for pancreatitis (1).  Additionally, a history of pancreatitis diagnosis and a comparison of the presenting symptoms to the historical symptoms is helpful.

BOWEL OBSTRUCTION
As the name indicates, this condition occurs when something obstructs the passage of fecal matter through the bowels.  This condition can result from chronic constipation, foreign object, or conditions like cancer or polyps.  Over half of the cases of large bowel obstruction result from the presence of cancer (1).  Patients generally present with episodes of increased pain during which bowel sounds are notably louder (even audible without a stethoscope).  The patient may present with abdominal distention (89% specific), previous abdominal surgery (94% specific) and constipation (95% specific) (1).  While these findings are fairly specific (positive findings rule in large bowel obstruction), they are relatively insensitive (a negative finding does not reliably rule out large bowel obstruction).  Making up 80% of bowel obstruction cases, small bowel obstruction is most often caused by post-operative adhesions (70%) (1).  For the purposes of the prehospital community, large and small bowel obstruction present with essentially the same findings in the history and exam.  Field treatment of bowel obstruction includes fluid resuscitation and pain management.

MESENTERIC ISCHEMIA
The small intestine is supplied with blood and nutrients by the mesenteric artery.  When this artery does not provide adequate circulation, ischemia of the small bowel can result.  While it can be caused by hypotension from hemorrhage in trauma (resulting in the “golden hour” – but that’s another post), the disease process here results from a clot blocking blood flow.  Other than abdominal pain, there are not many physical findings in EMS which can aid in a differential diagnosis of mesenteric ischemia.  If advanced, ischemia may result in decreased bowel sounds.  Often, patients will complain of pain much more severe than their physical finding would indicate (1).  A thorough history will serve the practitioner in this diagnosis.  Patients at high risk for clotting (history of atrial fibrillation, CHF, bed confinement, and recent surgical procedures) should be considered high risk for mesenteric ischemia (1).  Since the presence of mesenteric ischemia can be so life threatening, rapid transport should be considered if this disease process is considered likely.

CHOLECYSTITIS
Hopefully by this point we’re all on board with “-itis” meaning inflammation.  In this case we’re talking about the gall bladder and inflammation and pain specific to it.  The inflammation in question generally results from a prolonged blockage of the common bile duct, often resulting from gall stones.  The pain from cholecystitis is found in the right upper quadrant 54% of the time and in the epigastric region 34% of the time.  The pain generally comes and goes and is often cramping in nature,  radiating to the back, flank and chest (1).  For this reason, it is important to determine where the pain started before radiating and also to perform a 12 lead ECG for abdominal pain patients.

ABDOMINAL AORTIC ANEURYSM
An aneurysm is an out-pouching from an artery caused by a weakening of the arterial wall (see my post about CVA for some images of a cerebral aneurysm; same idea, different location).  In the abdomen, pain can be caused by an aneurysm of the abdominal aorta, a life-threatening condition requiring rapid assessment and treatment.  It is important to note that ultimately, the physical exam cannot totally rule out AAA from consideration.  One of the most important findings in the patient examination for ruling in AAA is orthostatic vital signs.  Since the patient often will not have large quantities of emesis or diarrhea, dehydration is ruled out as a cause of abnormal vital signs. A history of GI bleed symptoms (or lack thereof) will rule in or out that diagnosis as well. The classic presentation of AAA is historical hypertension, presenting with constant, severe abdominal pain, pulsating mass in the abdomen and profoundly positive orthostatic vital signs.  It is important to note, however, that for symptomatic AAA, a palpable mass is only present in 18% of patients (1).  For a ruptured AAA, the treatment is surgical.  Think of this as a trauma patient; the speed with which a patient can bleed out is staggering.  In this case, C3 transport is obviously indicated.

CONCLUSION
Abdominal pain is a frequent call for many EMS responders.  Given the breadth of possible causes, it is important for practitioners to keep a high index of suspicion for life-threatening causes.  Performing a thorough physical exam and history on patients with abdominal pain (even chronic ones!) will help to ensure that “must catch” diagnoses are caught.  Do your patients a favor and make sure that you give them the benefit of the doubt, particularly with a complaint as complex as abdominal pain.

CITATIONS

1 – Stern, Scott; Cifu, Adam; Altkorn, Diane. Symptom to Diagnosis:  An Evidence-Based Guide. New York:  Lange Medical Books, 2006.

2 – Lozeau, Anne-Marie; Potter, Beth. Diagnosis and Management of Ectopic Pregnancy. Am Fam Physician. 2005. 72(9): 1707-14.

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Filed Under: Assessment, Clinical Discussion, Medical Emergencies

Differential Diagnosis Series – Abdominal Pain (Part 1)

09/14/2010 by 510medic 3 Comments
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This post is the second in a series detailing the differential diagnosis process.  The first article reviewed the basics of differential diagnosis and this and subsequent posts will look at the process for specific complaints which frequently present to EMS.  This post is the first of two detailing the construction of a differential diagnosis for abdominal pain.  This article is also posted at my site:  510medic.com

INTRODUCTION
You are dispatched to a private residence 30 minutes before the end of your shift for abdominal pain.  What goes through your mind en route?  Aside from the obvious frustrations of course.  What symptoms do you think about on the way?  What possible diagnoses do you consider?  What concerns do have about the patient?

Abdominal pain represents one of our frequent calls in EMS. It is also one of the hardest complaints to diagnose.  The abdomen houses many organs, any of which could cause pain, and abdominal pain can be a symptom of serious conditions including cardiac disease and pneumonia.

DIFFERENTIAL DIAGNOSIS REVIEW
As discussed in the first article in this series, differential diagnosis is the method of evaluating data from examination and assessment to construct causes for presenting complaints.  An initial list is constructed based on the complaint or body system involved.  This list is narrowed down by findings that move the index of suspicion to the point that you are comfortable either treating or discarding that cause.  The usefulness of a test is quantified by specificity and sensitivity.  A positive result in a highly specific test means it is likely a patient has a certain disease.  A negative result in a highly sensitive test means it is likely that the patient does not have a certain disease.  Tests and assessments continue until your index of suspicion crosses the threshold to treat or ignore and you move to the next potential cause.

CONSTRUCTING A DIFFERENTIAL FOR ABDOMINAL PAIN
In building a list of causes for abdominal pain, the provider considers three important aspects:  the specifics of the pain, the patient’s history and the findings during the physical examination.  When reviewing the patient’s pain, the PQRST mnemonic (P – Provoke/Palliate, Q – Quality, R – Radiation, S – Severity, T – Time) can help to ensure than nothing is missed.  These findings, along with the location of the pain, can help construct a list of causes.  For instance, upper abdominal, or epigastric pain can be caused by the organs in that area:  the pancreas, gall bladder and stomach; though sometimes epigastric pain can result from a heart attack.  Knowing which organs are where is important because, for instance, pain from an appendicitis is likely to occur in the right lower quadrant so choosing that as a differential diagnosis for left upper quadrant pain could be a dangerous mistake.

Abdominal Organ Locations - via Flickr

Along with information about the patient’s pain, you should take a detailed history from the patient.  Knowledge of associated symptoms can aid in the construction of a differential diagnosis.  Some historical findings include:

  • Nausea/Vomiting
  • Diarrhea
  • Constipation
  • Change in oral intake
  • Blood in the stool/urine
  • Fever/Chills

By asking these questions, you are able to know the time frame of the symptoms and the organs or body systems affected.

In addition to symptoms associated with abdominal pain, it is vital to ask about the remainder of their medical history.  Particular attention is paid to respiratory symptoms and any cardiac history as abdominal pain may be a presenting symptom in both an acute myocardial infarction and pneumonia.  Lastly, the patient’s sexual/reproductive/menstrual history should be noted and any alcohol or drug usage.

The next step in the diagnosis of abdominal pain is the physical exam beginning with vital signs.  In addition to the standard set of vitals, consider checking for positive orthostatic changes (a drop in blood pressure and an increase in heart rate when moving from lying to sitting and sitting to standing).  Positive orthostatic findings include a systolic blood pressure drop of 20 mmHg or a heart rate increase of 20 BPM.  Care must be taken with patients on heart rate control medications (like Atenolol) because their heart rates cannot increase during times of shock.

Continuing the physical examination, the practitioner performs a cardiac and respiratory exam including 12 lead ECG, lung sounds and heart tones.  Since life threatening conditions like acute MI and pneumonia can present as pain referred to the upper abdomen or epigastric region, it is important to rule out the presence of these conditions early in the construction of a diagnosis.

Finally, the physical exam proceeds to the actual hands on assessment.  The patient is assessed through visual inspection of the abdomen, auscultation to check for the presence or absence of bowel sounds and palpation using first light pressure then deeper pressure.  During the palpation phase, it is important to talk to the patient to distract him and to work towards the region where the complaint of pain exists.

CONCLUSION
Based upon specific findings during the history and physical examination, the practitioner should be able to determine the underlying cause of the patient’s complaint.  In tomorrow’s post, we will present a review of some of the common causes of abdominal pain and which specific findings may indicate an underlying cause.  Stay tuned!

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Filed Under: Assessment, Clinical Discussion, Medical Emergencies

Treating Tachycardia

07/06/2010 by Adam Thompson, EMT-P 5 Comments
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Treating Tachycardia
By Adam Thompson, EMT-P

Tachycardia simply means a faster heart rate than normal.  With the sinoatrial node, which is the heart’s inborn pacemaker, the intrinsic rate is between 60 and 100 beats per minute.  When the rate exceeds 100 beats per minute, tachycardia is present.

When treating tachycardia, it is important to first consider a compensatory cause.  The body tends to use an increased heart rate as a frequent compensatory mechanism when it senses decreased perfusion.  Two of the best dysrhythmics in the EMT and paramedic’s tool box are OXYGEN and NORMAL SALINE. Both of these treatments should be attempted prior to using any other medication.  It is not advantageous to eliminate a compensatory tachycardia in a patient who needs it to perfuse.  Locating the cause of the decreased perfusion would be optimal.

Another thing to consider is the patient’s hemodynamic stability.  With organized tachycardic rhythms in unstable patients, synchronized cardioversion is indicated.  There seems to be a fear amongst prehospital providers when it comes to shocking people.  The paramedic seems to be much more comfortable giving anti-arhythmic/dysrhythmic medications than they do performing cardioversion.  This is in-fact backwards thinking.  Consider Kelly Grayson’s outlook on dysrhythmic drugs–they are selective cardiotoxins.  First off, they are not naturally found in the body.  Second, they metabolize over time and the reaction can be unpredictable.  Thirdly, they are used to counteract cellular depolarization.  Do you know what happens in the absence of cellular depolarization in the myocardium?  Asystole–not a common side effect, but it drives home the point doesn’t it?.  Other complications, like high-grade atrioventricular blocks, and long QT syndrome may also occur.  Conversely, synchronized cardioversion doesn’t have nearly as many unwanted effects.  It works fast, and goes away.  The medication you should be considering, is some sort of sedative or benzodiazapine prior to cardioversion.

Next, after determining the patient’s hemodynamic stability, the width of the QRS should be considered. If the patient is stable, and they are in a sustained tachycardia, dysrhythmic medications can be considered.  It is important to determine the width of the QRS, because medications like Cardizem (diltiazem), or Adenocard (adenosine) that may be administered to narrow complex rhythms, can effectively KILL people with wide QRS rhythms.  Notice that there is not a ‘ventricular tachycardia’ algorithm?  It states ‘Wide QRS’, and lists ‘uncertain rhythm’ below.  This is an important concept.  If it is wide, and you are uncertain of the origin, it is ventricular tachycardia until conclusively proven otherwise.  Another reason that it is a WCT guideline and not a ventricular tachycardia guideline is because of conditions like WPW (wolff parkinson white syndrome).  With WPW, a delta wave may be present causing widening of the QRS complex.  This is important because adenosine, and Cardizem should not be administered to patients with WPW.  There is controversy regarding whether Amiodarone is safe with WPW, but as of now the American Heart Association considers it a safe option.

A wide QRS complex is considered greater than 120 ms or 0.12 seconds or 3 small boxes.

Points to remember:

  • O2 & fluids for compensatory tachycardia
  •  Synchronized cardioversion is the SAFER option
  • If QRS is wide treat as V-tach
Note: Torsades de Pointes should not be treated with Amiodarone.  This can cause lengthening of the QT interval, and subsequently a worse arrhythmia.  

Brugada Criteria.  This should only be used to confirm ventricular origin.  Not to rule it out.  

View more documents from Adam Thompson.

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Filed Under: Cardiology, Education, Medical Emergencies

When All You Have is a Hammer, Every Problem Looks Like… Lasix?

06/22/2010 by Adam Thompson, EMT-P 1 Comment
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I posted this article over at http://www.lifeunderthelights.com/ a few days ago and I thought it would good for here as well. I’m sorry that I’ve only rarely posted here, but I read this blog quite often and recommend it to all of my peers. Enjoy

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A few years ago I responded to a structure fire on the main engine out of my station. The fire was at a house that had been converted to a dog kennel and grooming shop just a few blocks away from the firehouse and was a short response time. It was a light-staffing day and we responded as a three person engine company. As the senior firefighter I was the acting company officer and my new girlfriend at the time, who just happens to be my wife now, was the backseat firefighter. Get ready for the “Awwww” moment… it was our first fire “as a couple”. There was a number of cool things that came out of the fire, but one of them was the fact that Gina grabbed *my* maul.

On our main engine, there’s an 8-pound maul (big hammer) that I grab as my tool of choice every time I jump off the truck for a fire. It just tucks so neatly in my SCBA’s belt and is so compact yet handy that I make a beeline for it every time. This time, Gina had taken it, so I grabbed a pick-head axe.

It’s amazing when I have my maul how every access problem looks like something that I can solve by whacking it with a hammer of some sort. On this fire, I learned that when one has an axe, every problem looks like it can be solved by some sort of chopping.

Moral of the story, Gina and I entered the structure, saved the pooches, and stopped the fire in its trucks with minimal damage. There’s actually a hilarious video that I believe is still on our department’s web site that I’d let you see if I didn’t hide the name of the department(s) I work for due to reasons of wanting to remain employed.

And, like a lot of posts I write, I told you that so I could tell you this about an EMS call I responded to an indeterminate amount of time ago. I have the honor and privilege to be the senior medic on most shifts I work and I precept a lot of students on the ambulance. This shift was no different and this 0-dark-30 call illustrates a point that I’d like to explain to you.

For this call, the primary ambulance out of our station responded because they were on the way back from another call and my partner and I responded in our ambulance because we were up on the alternating call rotation. They arrived at the poorly-accessible apartment complex a few minutes before we did and made first patient contact. As it turns out, the middle age patient had ran out of his/her prescription Lasix (a potent diuretic, or water pill) a week or so prior to the call and had been retaining a great deal of excess bodily fluid. The patient’s legs were markedly and grossly swollen and weeping fluid out of fluid filled blisters. The Patient called us because he/she could no longer stand the pain of the cellulitis (infection) that had developed. The patient had no respiratory compromise, his/her lungs were clear, and he/she really had no other complaints. The patient had an extensive medical history of organ failure and disease. He/she was fully alert and oriented, and was able to assist us as we simply picked him/her up and carried him/her to the cot.

As we were loading the patient up in the ambulance and I was about to get into the back to continue my assessment and treatment of the patient, the EMT from the other ambulance who happens to be an almost-done Paramedic student told me, “So those legs are the worst I’ve ever seen fluid wise, you’re going to push some lasix on this one”. I mumbled something and got into the truck. I was tired and wasn’t really able to form complete sentences at the time due to sleep deprivation. I continued my assessment where I found that the frail patient had a blood pressure in the 70 systolic range (Low!) and that in addition to retaining fluid in his/her legs, he/she was also retaining fluid in his/her abdomen and was probably in need of a paracentesis. I managed the patient with a (beautifully executed, I must say) IV stick into an impossibly small and crooked vein, and gave just enough fluid to bring his/her BP up a bit without adding to his/her fluid overload all that much. I put the Pt on oxygen and a cardiac monitor, which revealed a normal sinus rhythm without ectopy and obtained a 12-lead EKG as well, which was not indicative of any acute problems. The patient stated that his/her pain was managed by padding and positioning of his/her swollen legs and even though he/she complained of no breathing problems, I put him/her on a bit of oxygen via nasal cannula.

The transport was uneventful, although his/her blood pressure never did come up. The ER later diagnosed the Pt with complete liver failure and toxicity.

But the interesting part of the story is this, when I got back the medic student asked me about giving IV lasix to the patient, as we carry that in our medication stock and have it available as an emergency diuretic for patients in congestive heart failure and/or fluid overload with pulmonary edema and respiratory compromise. He was almost taken aback when I said that I didn’t give any.

I asked him if he did a full assessment. He said that he had tried… but that he didn’t have enough time before I arrived and we took the patient out to the ambulance. I gave him my assessment findings and the news of the very low blood pressure. He said that he agreed with me on not giving the lasix with the markedly low blood pressure but was curious when I explained that it wasn’t the reason I didn’t give the medication.

We in EMS, and especially new providers carry our own hammers… our treatments and medications that we’re able to give in the field. Medics that use these treatments more often are called “aggressive” and it is a badge of honor. In fact, in some cases, aggressive field treatment is indeed warranted and improves patient outcomes. However, in a lot of cases it is not indicated and patients benefit from what we don’t do more so than from what we could have done.

This patient didn’t have any respiratory compromise and while he/she obviously could have benefited from the dieresis or removal of the excess fluid, she didn’t meet the criteria for emergent field administration of lasix, which is respiratory compromise from pulmonary edema. I made the decision to let the physician evaluate the patient and determine the best treatment path that would fit in with the patient’s ultimate plan of care. I didn’t believe that the patient would ultimately benefit from my administration of lasix twenty minutes earlier than the ER could have done it if the physician so chose.

Every treatment we administer must be given with a full assessment of the risks and benefits to the patient for doing so. Every EMS person should familiarize themselves with the long-term care paths of the conditions we treat and try to maximize the long-term benefit to the patient with the acute and short-term care we give. Not every problem is “a nail” and sometimes the hammers we carry aren’t the best ultimate solution for excellent patient care. Remembering how we as EMS people fit into the grand scheme of the overall healthcare system and in the ultimate care paths of our patients will help us all to do what we’re supposed to do, which is to provide excellent and appropriate patient care.

It is also of note, I guess, that Gina rarely steals my maul anymore. Now that we’re married… I “give it freely” to her.. What’s mine is her’s, as they say.

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The original post has some pictures of the fire and of the doggies that my wife and I saved on our first “Fire Date” – It can be seen HERE

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Filed Under: Case Reviews, Clinical Discussion, Critical Judgment, Education, Medical Emergencies, paramedics, Pharmacology

Alcoholic Emergencies

10/11/2009 by Adam Thompson, EMT-P Leave a Comment
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That Drunk May Be More Than Just Drunk

by Adam Thompson, EMT-P






In prehospital emergency care, it is not uncommon to come across an intoxicated patient from time to time. We usually look at our partner with a smug and I’ve-had-enough manor and just say “E-T-O-H”. EtOH stands for ethanol, which is a medical way for us to say alcohol without the patient thinking we are judgmental–even though we are. These patients may be the nicest patients or the meanest. They may say things to you that might make you want to send them from a standing to supine position. You may even want to do worse. Put the 16 gauge IV catheter away and empty that syringe you have filled with succs–I know it’s tempting.

These patients are actually presenting with a form of altered mental status that we are writing off as drunk guy. You probably check a sugar on these patients because your EMT or paramedic instructor explained to you the common misdiagnosis of ketones for alcohol, and they may even teach this in online medical coding courses. So you try to rule out a diabetic in DKA even though you see two empty bottles of Jim Beam on the nightstand. You are also probably aware of the need for Thiamine with the administration of dextrose to these patients. Even though this patient might not be in DKA or hypoglycemic, he may be having a medical emergency.
Myth: Alcohol on the breath smells similar to ketones
Truth: Those are ketones
Drinking alcohol leads to a production of ketones through an oxidation process and you emit the fragrance of ketones.
It is often that chronic alcoholics will supplement food for alcohol. When they do this, they are subsequently getting all of their nutrition from the alcohol and the fats in their own body. Similar to a diabetic in DKA, these patients will go into a state of ketosis to get their body some energy. Ketosis is the state in which lipids (fats) are broken down for fuel. Ketones are produced. Those ketones are acidic, and that is where we get that lovely term ketoacidosis. These patients are suffering from a malnourished emergency, and should be treated accordingly.
Wernicke’s Encephalopathy
Encephalopathy = Brain damage
Thiamine (vitamin b1) deficiency can lead to a condition known as Wernicke’s Encephalopathy. This condition is characterized by ataxia, ophthalmoplegia, confusion, and impairment of short-term memory.
Ataxia – Gross lack of coordination of muscle movements. You know, like a drunk stumbling around.
Ophthalmoplegia – Paralysis of one or more of the extraocular muscles which are responsible for eye movement. Have your patient look left, then right.
When Wernicke’s encephalopathy is accompanied by Korsakoff’s syndrome, it is referred to as Wernicke-Korsakoff’s Syndrome.
eMedicine [link]

Studies suggest that up to 80% of patients with Wernicke encephalopathy may not be diagnosed, which makes estimates of mortality rates unreliable. Wernicke encephalopathy is a significantly disabling and potentially lethal condition that can be prevented or reversed if treated early. Established Wernicke encephalopathy can have major long-term consequences among patients requiring permanent institutional care.

Other Possible Signs & Symptoms:
  • Hypothermia
  • Weakness
  • Foot droop
  • Decreased proprioception
  • Nausea/Vomiting
  • Abdominal pain
  • Hypotension
  • Coma
Possible Causes:
  • Prolonged alcohol abuse
  • AIDS
  • Hemodialysis
  • Infection
  • Starvation

Treatment = Thiamine and fluid replenishment

Pubmed [Link 1]

Wernicke encephalopathy is caused by thiamine deficiency in the central nervous system, and is defined by the triad of confusional symptoms, ocular alterations and ataxia. Some other factors may also predispose alcoholic patients to this deficiency. We report two patients with hyperglicaemia and ketoacidosis due to diabetes mellitus decompensation and chronic alcoholism who developed Wernicke encephalopathy before their hospital admission. The outcome was successful after intravenous thiamine administration and insulinotherapy. The presence of Wernicke encephalopathy in alcoholics with diabetic ketoacidosis, suggests that metabolic decompensation is essential in the onset of the disease.

Pubmed [Link 2]

BACKGROUND AND PURPOSE: Wernicke encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke encephalopathy with and without a history of alcohol abuse. MATERIALS AND METHODS: A multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke encephalopathy. The age range was 6-81 years (mean age, 46 .6+/-19 years). RESULTS: Fifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group. CONCLUSIONS: Our study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.

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