Case 20 Questions
1. Which is true for metacarpal fractures?
2. Which is true of carpal fractures?
3. The most likely complication of the above injury includes…
Filed under: radER
Case 20 Questions
1. Which is true for metacarpal fractures?
2. Which is true of carpal fractures?
3. The most likely complication of the above injury includes…
Case Presentation by Dr. Arun Rajasekhar, MD
CHIEF COMPLAINT: Right leg injury.
HPI: A 43-year-old man stated that another person landed on his right leg. He felt and heard a snap and then he immediately experienced severe right knee pain. This happened within 1 hour prior to admission. He was brought here by EMS. He complains of severe right knee pain. He has not done anything for his symptoms.
PAST MEDICAL HISTORY: Denies diabetes, seizures, hypertension.
VITAL SIGNS: Blood pressure 184/86, pulse rate 93, respirations 20, temperature 36.3.
GENERAL: This is a well-developed, well-nourished 43-year-old man, awake, alert but uncomfortable due to pain.
MUSCULOSKELETAL: Normal muscle bulk and tone. He has a deformity of the right knee. He has normal dorsal pedis and posterior tibial pulses. He has good popliteal pulse. He has a deformity of the right knee.
1) The above xray shows anterior displacement of the tibia on the femur. Which ligament is most likely to have been completely torn?
2) Which of the following is NOT a hard sign of vascular injury associated with knee dislocations
a) absence of pulse
b) expanding hematoma
c) paresthesias in leg
d) bruit over site of wound
3) Patient required conscious sedation for reduction of his knee. Decision was made to use ketamine and propofol. Immediately after infusion, Pt starts gasping for air and immediately becomes tachycardic and tachypneic. He has equal breath sounds. Trachea is midline. What is your working diagnosis and which of the two agents is most likely responsible? What should be done?
a) Acute tension pneumothorax due to propofol administration. Needle decompression
b) Acute laryngospasm secondary to ketamine administration. Paralyze patient and intubate immediately
c) Acute laryngospasm secondary to propofol. Attempt to bag patient through laryngospasm
d) Acute laryngospasm secondary to ketamine. Perform cricthyrotomy.
Answers & Discussion:
1) A & D
1) PCL and ACL are both acceptable answers. The patient has an anterior knee dislocation. This is the most common type of knee dislocation. It is caused by hyperextension of the knee joint. Often both he PCL and MCL will be torn. With all knee dislocations it is important to have a high index of suspicion for popliteal artery injury. Initial assessment of the leg should include palpation of the dorsalis pedis and popliteal pulses. You can also perform ABIs to assess distal blood flow. It is important to note that PT and DP pulses will be normal in 5-15% of popliteal artery injuries. CT angiography can be used to detect arterial injury.
2) Parasthesias is the answer. Hard signs of vascular injury include active hemorrhage, expanding hematoma, bruit over wound, absent distal pulses, extremity ischemia (cold to touch, paralysis, pallor). In the setting of penetrating trauma, hard vascular injuries are 100% predictive of arterial injury and patient should be taken directly to operating room for surgical exploration. In the setting of blunt trauma, hard signs are less reliable and false positives are common. Repeat physical exam should be performed after resuscitation and reduction or orthopedic injury. If hard sign persists, get CT scan. Diagnosis of popliteal artery injury is time sensitive. Amputation rate increases the long repair is delayed. Rate of amputation is 90% eight hours out from the time of injury.
3) Patient is experiencing acute laryngospasm secondary to ketamine. This is a rare but known side effect of ketamine. It has been primarily reported in the pediatric literature. Patient’s will desaturate and decompensate quickly. In my scenario, the patient had a very visible reaction to the medication but there have been case reports of patients desaturating without showing a obvious signs of distress because of the sedative effect of the ketamine and the propofol. If a patient begins to desaturate and you are uncertain as to the exact etiology, the first and simplest thing to do is a jaw thrust maneuver to see if that relieves the hypoxia. You can also bag mask the patient. However, neither of these maneuvers will relieve laryngospasm. This patient needs neuromuscular blockade to relieve the laryngospasm and once the patient is paralyzed you should immediately proceed to intubation. Some sources stated that you could bag mask the patient until the paralytic wears off but I think if you are going to paralyze a patient, then you should give them a definitive air way.
CC: “My chest hurts”
HPI: The patient is a 56yo female who presents to the emergency department as a medical code for tachycardia. She is well known to the emergency department for multiple admissions for DKA. The patient is complaining of chest pain that started earlier today, however, is unable to provide us with any more history due to confusion. She is thrashing on the stretcher, moaning, and not fully responding to questions.
ROS: Unable to obtain secondary to medical condition
Past medical history: Diabetes mellitus with multiple admissions for DKA, glaucoma, hypertension, renal insufficiency, chronic anemia
Past surgical history: Unknown
Social history: Per EMR positive history of remote drug abuse.
Family history: Diabetes
Medications: Reports she is compliant with her Insulin 70/30 10U BID, other medications unknown
PMD: She states she has no regular doctor
- T: 36.0 – orally
- P: 119
- BP 124/70
- R 20
- O2 sat 98% RA
GENERAL: The patient appears agitated and is hyperpnic. She is wearing clothes that appear dirty and have holes in them. She does open her eyes spontaneously, she is unable to coherently answer questions, however, is moaning in response to questions and pain.
HEENT: Head normocephalic, atraumatic Conjunctivae are pink without pallor. Pupils are 3mm bilaterally, equal, round and reactive to light.
NECK: Supple. Trachea midline.
HEART: Tachycardic rate, regular rhythm, no murmurs, rubs or gallops
LUNGS: Lungs are clear to auscultation bilaterally, no wheezes, rales, or ronchi, increased ventilation, no retractions or use of accessory muscles.
ABDOMEN: The abdomen is soft, nondistended. It is diffusely tender to palpation no rebound or peritoneal signs, no increased tenderness at McBurney’s point, negative Murphy’s sign.
EXTREMITIES: Dorsalis pedis and radial pulses are 2+ bilaterally. No pedal edema.
NEUROLOGIC: The patient is alert. Her face appears symmetric. She smiles and closes her eyes symmetrically. She responds to some commands and moving all 4 extremities with good strength and purpose. We are unable to evaluate her speech at this time, since she is moaning in response to questions.
In the resuscitation bay, the patient was immediately placed on an O2/cardiac monitor, which revealed an O2 sat of 98% on room air and sinus tachycardia. Nursing staff placed two large bore peripheral IV lines and basic labs were drawn. Two boluses of NS were started wide open. Accucheck revealed a CBG >600.
Chest XR revealed no pneumothorax or pulmonary infiltrates.
BMP: Na 142, K 4.7, Cl 91, HCO3 5, BUN 42, Cr 2.25 BG 1,037
CBC: WBC 11.4, Hgb 9.6, Hct 31.5, Pl 438
Beta Hydroxybuterate: >100
Question 1: What is the most likely cause of this patient’s change in mental status?
Question 2: In the treatment of DKA, what is the ABG pH for which bicarbonate therapy is recommended?
A) pH < 6.8
B) pH < 7.0
C) pH < 7.1
D) pH < 7.3
Question 3: In a diabetic patient with refractory hypoglycemia, what medication are you most suspecting responsible for this finding?
Part B: Name a treatment for hypoglycemia associated with Type II DM (not glucose in any form).
Answers & Discussion
Question 1: C. The pathophysiology of DKA involves concurrent insulin deficiency and glucagon excess that combine to produce a hyperglycemic, dehydrated, acidotic patient that has profound electrolyte abnormalities. Although all of the above can contribute to altered mental status, the most important factor is hyperosmolarity, a result of hyperglycemia and dehydration. The renal tubules begins to excrete glucose in the urine (glycosuria) when the blood glucose reaches a level above 160-180 mg/dl; the proximal renal tubules become overwhelmed at that level and are unable to resorb the excess glucose. The excess glucose in the renal tubules draws water and other electrolytes, via an osmotic effect, into the urine. This osmotic diuresis along with dehydration from poor oral intake and vomiting promotes hyperosmolarity and altered mentation. Ketoacidosis is also an important factor that can determine mentation, however, it has a contributory effect with hyperosmolarity, rather than absolute effect on its own in DKA.
The formula for serum osmolality is = 2(Na+) + Glucose/18
One must be very careful when interpreting the laboratory values in a patient with suspected DKA. The serum sodium levels are often misleadingly low in hyperglycemic states. In profound dehydration, sodium levels are usually on the lower end secondary to hyperglycemia, hypertriglyceridemia, low salt intake, increased GI/renal losses, along with perspiration/insensible losses. The pathophysiology of falsely low sodium is due to water flowing from cells into the intracellular space due to the marked hyperosmolarity, creating a dilutional hyponatremia. The true value of sodium can be calculated by adding 1.3-1.6 to the sodium lab value for every 100mg/dL of glucose above the normal value. This calculation cannot be accurately used, however, if profound hyperlipidemia is noted. Hypertriglyceridemia is a common finding in DKA, owing to the fact of impaired lipoprotein lipase activity and overproduction of hepatic VLDLs. These lipids further promote dilution of the blood and falsely decrease sodium concentrations.
Question 2: B. The use of bicarbonate therapy in treating DKA is controversial. Successful treatment of DKA involves correction of dehydration, hyperglycemia, and electrolyte imbalances. Initially, ABCs should be established. The initial fluid therapy is directed toward total intravascular volume expansion as well as restoration of renal perfusion. Typically, normal saline is used at a rate of 15-20ml/kg /hr. If the patient is in hypovolemic shock, more fluids may be necessary. If the patient has other co-morbidities, such as heart failure or CKD, it is important to monitor the patient hemodynamically so to not fluid overload the patient.
In general, insulin administration shuts of ketogenesis and in turn will correct the acidosis. Bicarbonate therapy is generally not recommended by the ADA, unless the pH is below 7. Bicarbonate therapy has not been shown to improve outcomes and has actually been shown to worsen prognosis in patients with pH ranges of 6.9-7.1, and in fact, lower pH has been shown to directly inhibit further ketogenesis via a feedback mechanism. Bicarbonate shifts the oxygen-hemoglobin dissociation curve to the right via 2,3-DPG deficiency, worsening oxygen release in tissues. Also, quickly correcting the intravascular acidosis will terminate Kussmaul respirations, allowing the CO2 to cross readily into the brain circulation across the blood-brain barrier, making CSF acidic. In addition, administration of bicarbonate will drive potassium further into the cells, making hypokalemia even more pronounced. Finally, overaggressive use of bicarbonate administration may produce alkelemia later on in the treatment course, secondary to ketones being metabolized into CO2, water, and bicarbonate.
This is a guideline and the complete clinical picture should be considered, not just a number.
Question 3: B. Hypoglycemia is a major and most dangerous complication associated with both type 1 and type 2 diabetes. Severe hypoglycemia is typically defined as blood glucose levels below 40-50mg/dL associated with altered mentation. It occurs when patients use too much insulin/oral hypoglycemic medication and either have decreased oral intake, increased energy expenditure, or increase their insulin dosage. Patients that have had multiple bouts of hypoglycemia may become immune to the warning symptoms, causing what is known as hypoglycemia unawareness. This in turn can result in significant morbidity and mortality. Since their blood sugar can plummet without their awareness, these patients may become unresponsive and unarousable very quickly and without warning. Signs and symptoms of hypoglycemia are a result of adrenergic drive of epinephrine. These signs and symptoms include sweating, nervousness, tremor, tachycardia, and altered mentation.
Pioglitazone and Rosiglitazone are within the thiazolidinedione class of oral hypoglycemics. This class of medications reverses insulin resistance of the muscle and fat cells, and also acts on hepatocytes to a lesser degree decreasing gluconeogenesis. Hypoglycemia is not a known side effect of thiazolidinediones. Glyburide, on the other hand, is a longer acting oral hypoglycemic belonging to the sulfonylurea class. This class of hypoglycemics is known to cause hypoglycemia, especially after exercise or missed meal, after being discharged from the hospital, with use of longer acting medications, and malnourished patients, amongst others. This class of medications increases insulin release from the beta cells of the pancreas at any blood glucose concentration. Metformin does not typically cause hypoglycemia because it only works when there is a baseline insulin level within the body. It acts to increase insulin’s action rather than to stimulate its release.
Patients with suspected overdose on oral hypoglycemic agents should be observed for 24 hours if hypoglycemia recurs after initial treatment in the ED. Patients that are most at risk for refractory hypoglycemia are those with impaired renal function, pediatric patients, and those patients who have just been started on an oral hypoglycemic.
In addition to frequent glucose monitoring and replacement, treatment with an agent to inhibit insulin release, like octreotide (a somatostatin analogue) canbe used. The recommended dose for adults ranges from 50-100 mcg IV or SC every 12 hours. In fact, giving patients multiple doses of D50 to raise their blood sugar in turn will stimulate more insulin to be produced, given the sulfonylureas still in the system. Although the exact mechanism of action is not known, Octreotide will block the insulin release that is caused both by the sulfonylureas and dextrose.
Prior to discharge, a meal should be given to the patient to make sure that the patient can tolerate oral feedings and this meal can begin to replenish the glycogen stores. Close outpatient follow-up is necessary to re-evaluate the oral hypoglycemic agent dose.
Conn’s Current Therapy 2014 Edward T. Bope, Rick D. Kellerman; Elsevier Inc, 2014
Rosen’s Emergency Medicine
Kitabchi A, et al. Hyperglycemia Crisis in Adult Patients with Diabetes. Diabetes Care, Volume 29, #12. December 2006.
Case Presentation by Dr. Tim Scott, DO
CHIEF COMPLAINT: “MY chest hurts”
HISTORY OF PRESENT ILLNESS: 62yo white male presents from home with chest pain. He states it is substernal and non-radiating and started 30 mins prior to arrival while he was helping his wife in the garden. He was kneeling down cutting thorns off of a rose bush. It states it felt like indigestion and he tried to burp a couple of times but it did not help. It was 8/10 initially and is now 6/10. He went in the house and sat down and drank a glass of water but this did not help. He takes an aspirin daily and did not try any other medications. He states he feels a little sweaty and light headed but denies any other symptoms. Otherwise usual state of health. States he has hypertension, no previous history of heart attack or coronary artery disease he is aware of.
REVIEW OF SYSTEMS:
Constitutional: Denies weight losst
Cardiovascular: Denies palpitations or syncope
Respiratory: Denies hemoptysis
Gastrointestinal: Denies rectal bleeding
Genitourinary: Denies hematuria
PAST MEDICAL/SURGICAL HISTORY: HTN – only surgery was tonsillectomy many years ago
SOCIAL HISTORY: Pt denies smoking, socially drinks alcohol and denies ever using any illicit drugs
EXAMINATION OF ORGAN SYSTEMS/BODY AREAS:
VITAL SIGNS: Blood pressure 106/54, pulse 92, respirations 20, temperature 36.3, SpO2 95% on RA
GENERAL: Well-developed, well-nourished, alert and oriented x3 and mildly uncomfortable secondary to acute condition.
HEENT: Head is normocephalic and atraumatic with no gross signs of trauma. The pupils are equally round bilaterally with extraoccular movements grossly intact and no conjunctival pallor. Sclera are icteric and non-injected. Mucous membranes of the mouth are moist without erythema.
Neck: No adenopathy. Trachea is midline.
LUNGS: Clear to auscultation bilaterally without wheezes, rales or other adventitious breath sounds. Good airflow, no accessory muscle use.
HEART: Regular rate and rhythm. S1-S2 noted. No clicks rubs or gallups auscultated. No murmurs auscultated.
ABDOMEN: Soft, non-tender, non-distended. No pulsatile masses appreciated.
MSK/EXTREMITIES: Normal strength bilaterally in upper and lower extremities. Peripheral pulses are present and symmetric bilaterally at 2+ in all extremities. Homan sign negative bilaterally. Good pulses at radial and posterior tibial arteries bilaterally
Skin: No edema. Warm and moist. No calf erythema.
NEURO: Patient is awake alert and oriented x3 with normal speech and normal hearing. Patient is responding and cooperating appropriately to exam. Face is symmetrical.
Pt placed on a cardiac monitor and 2L O2 via NC and an IV is established with an accucheck performed before you ever see the patient (yes, you are at an outside institution … a very rural ED to be exact). The nurse grabs you because the monitor looks funny. You agree and order a 12 lead EKG. You are handed the following gem:
Lucky for you, the cardiologist happens to be in the ED seeing another patient. You grab an old EKG which shows an obvious LBBB and you show this new one and the old one to the cardiologist. The cardiologist tells you to go ahead and admit to him for “repeats and serials” …
It is a perfect world. You have mentally ruled out PE and Aortic Dissection and you are right.
1) Your next step is to …
A: Give the patient 325mg ASA PO. Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR.
B: Give the patient 325mg ASA PO. Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR. Perform a rectal exam with FOBT and start the patient on Heparin.
C: Give the patient 325mg ASA PO. Order CXR and labs including CBC, lytes with BUN/Cr, troponin now and 3 hours from now, PT/INR. Perform a rectal exam with FOBT and start the patient on tPA via STEMI protocol
D: Give 325mg ASA PO. Repeat an EKG in 15 minutes and evaluate for evolution of suspected acute ischemia.
2) If you agree with the cardiologist, you know you will be monitoring the patient until the first troponin comes back. At that time, if it is elevated you know this cardiologist will want you to transfer the patient to a place that can do an interventional left heart cath and has a CCU. If you didn’t agree with the cardiologist and pushed tPA you know you have to do the same. Either way, you know you have to consider your transfer options. You ask the secretary to find out if flight is available today (yes they do these things) and what your ground crew options are. She tells you that you have BLS and ALS ground, no ICU transfer via ground team. You have fixed-wing and helo both flying and available at both can be to your hospital and ready to ship in equal amounts of time. Should you need to transfer this patient, what will you choose and why?
A: ALS ground because the first troponin came back at 0.125 and you and your cardiology friend decided this was a classic NSTEMI but he is scared to admit so you have to transfer the patient to a tertiary care center
B: ALS ground because you immediately pushed tPA and the crew can be there 30 minutes quicker than the helo team. Time for ground transport is 1hr 45 minutes.
C: Fixed-wing because you immediately pushed tPA and you feel that it is safer than helo (though it may take slightly longer overall).
D: Helo because you immediately pushed tPA and you feel it is the fastest.
3) Which of the following is NOT an indication for Air Medical Transport (AMT)?
A: Use of local ground transport would leave the local area without adequate EMS coverage.
B: Based on information available at the time and your best clinical judgement, you determine need for AMT.
C: The roads are icy and it is late at night. Ambulance driver says “I can do it, but I don’t like it”.
D: The interventional cardiologist at the tertiary care center was screaming in your ear on the phone “YOU HAVE TO SEND THIS PATIENT HERE ASAP in a HELICOPTER!!!!!!”
E: Local ground crew says “sorry doc, we cant go more than 100 miles” (tertiary hospitals is 150 miles away)
4) PCI and thrombolytics are the standard of care for treatment of acute STEMI. One of the known complications of either one of these is a reperfusion injury which is though to be induced by the restoration of blood flow to previously ischemic tissue as the reintroduction of oxygen and energy into a now anaerobic and acidotic environment can lead to further myocyte damage. Which of the following are true regarding coronary reperfusion? (More than one acceptable answer)
A: ST-segment normalization and terminal T-wave inversion in the first hour after thombolysis are poor and clinically insignificant indicators for reperfusion
B: Factors contributing to reperfusion injury include: mitochondrial damage, myocyte hypercontracture, free radical formation, inflammatory mediators, platelet activation and complement activation
C: The arrhythmia that is most commonly associated with reperfusion is atrial fibrillation.
D: Ventricular tachycardia and ventricular fibrillation can also occur after thrombolytic therapy; however, these arrhythmias are more likely to reflect persistent occlusion and infarction than a reperfusion injury … but more importantly, they are the most common cause of spontaneous death in the reperfused patient and sphincter tone should elevate to catastrophic levels when this is encountered.
Answers & Discission:
4) B & D
1. C – This is a STEMI. Clinically and electrographically this is a STEMI. Using Sgarbosa and/or modified Sgarbosa criteria, this is a STEMI. Your sister in third grade thinks this is a STEMI. You are 150 miles from a tertiary care center so you must do something to attempt to treat this STEMI until you can get them to the definitive spot. You should tell your nurses to initiate the in-house STEMI protocol. Give the patient 325mg of ASA. Ask the clerk to get whatever interventional cardiologist on the line that your hospital has a transfer agreement with. Tell them you will be giving ASA and thrombolytics (unless you encounter an absolute contraindication) and transporting the patient to them. Ask them if there is anything else they want. Hang up. Go through the tPA checklist, making sure there are no absolute contraindications. Explain the risks and the benefits to the patient. This can be as easy as saying: “Risks include bleeding in your gut, your chest and your head. You could die or become permanently disabled from this medication. Benefits: Those things I said rarely happen and you have also have a chance (somewhat higher) of dying if you don’t get this medication.” DOCUMENT that you did all this. (At the end of all of this, don’t forget to document your critical care time minus all billable procedures as well… I digress)
2. D - How to transfer a patient can be one of the toughest decisions to even the most seasoned physician. There are multiple modalities, most of which are listed above and pretty self-explanatory. The correct answer here is D. Helo is fast and though it is dangerous, ambulances and airplanes crash too. If the skies are clear and the team is available to fly helo, it is no doubt the fastest form of travel (with rare exception) and in stroke and STEMI which are the most common time sensitive conditions requiring medical transport, time is tissue and it is your job to get them where they need to be. A is wrong because this is NOT an NSTEMI. B is wrong because the helo or fixed-wing transport will still be quicker than ambulance in this scenario despite the initial delay. C is wrong because helo is faster. Fixed-wing is ARGUABLY safer but it is slower and anything can crash. If you still want to argue with me and say “Fixed-wing isn’t that much slower and I think the benefit of less fixed-wing crashes outweighs the risk of the small time delay vs helo” … then I say fine. When you are out there, you can make whatever decision you want but think of this. You have a very important morning meeting today and you woke up late. If you arrive late to this meeting, you might die. You don’t have to get on the national transportation safety website to know that more car crashes and vehicular deaths occur on the expressways than the surface streets every year. You know your risk of crash and death is higher if you take the expressway. Are you really going to take the back roads? …. I have included some more information for your leisurely reading on the types of transport teams.
BLS bus usually staffs EMT-B and refers to the use of emergency care without the use of advanced therapeutic interventions and includes airway management (oral and nasal, BMV), CPR, hemorrhage control, fracture and spine immobilization, and child birth assistance. They often have an AED as well.
ALS bus usually staffs EMT-I, EMT-P or equivalent and offers more comprehensive service such as an advanced airway, IV line placement and medication distribution en route, cardiac monitoring and manual defibrillation and certain invasive procedures.
ICU transport varies considerably but in generally you want this team when the patient is intubated, or you have a high index of suspicion they could need it en route (though if this is the case more often than not you should intubate before you send them out). ICU transport teams can run a vent and manage drips such as pressors, paralytics and sedatives and vasoactive agents. Almost all flight crews are staffed by an ICU team.
3. D is an incorrect answer. A, B, C and E are all true statements. I will refer you to Box 191-3 from Rozen’s
A refers to #8 and is self-explanatory. B refers to #9. Remember you are the one with the training and the knowledge. There might be a million protocols and suggestions out there but it is your job to integrate all things available to you from patient history, presentation and condition to hospital and city policies to what may happen on the way, to where the patient is going. You have the full clinical picture, you make the call. C refers to # 1 and 2. Your ambulance driver knows these roads and he/she has probably made the trip you are sending them on many times. If they are suggesting to you that they don’t think the drive is safe for some reason or another, don’t let them be a hero. Explore your next option. D refers to #9 again and look at my previous explanation. The cardiologist doesn’t make the call, you do.
4. B and D are correct.
There is a very good discussion of reperfusion injury on UpToDate, which is where I pulled this info from. I’m not going to copy and paste it but I highly suggest you read it. I don’t usually like UpToDate and you will rarely hear me say something good about it, but this article is a solid 30 minute read.
A is wrong. ST segment normalization and terminal T-wave inversion within the first hour are good markers for reperfusion. You can argue which is better, but that isn’t the question. Please pay attention to your patient first and foremost, they are a pretty good marker too for what is going on post thrombolytics. If they say “I don’t feel good, something isn’t right”, be scared. Don’t walk away yet. Watch the monitor and watch them and charge some paddles.
B is correct. These are all pathologic causes of reperfusion injury. Cell ischemia gets the ball rolling and nature does the rest.
C is wrong. An accelerated idioventricular rhythm (AIVR) is the most common arrhythmia seen with reperfusion after thrombolytics. AIVR usually pretty easy to distinguish on the monitor but you have to be thinking about it or you will be tricked into thinking it is a standard BBB. Basically an AIVR means a rhythm being paced by the ventricles. Now anytime you have a ventricularly paced rhythm you can count on a wide QRS so you know this will be present. And normally, ventricles would pace at less than 50bpm, so in AIVR you have a rate >50 and a wide QRS with a BBB morphology. More often than not, it is originating from the left ventricle. One more caveat, if the rhythm is driven by the ventricles and the rate goes greater than 120, you are out of the realm of AIVR and you are now talking Vtach (and be ready for Vfib, either way, get ready for some electricity and draw up some amiodarone, you might need both soon).
Recap of this. AIVR is the MC reperfusion arrhythmia and is characterized by a wide QRS and a rate greater than 50 but less than 120.
D is correct. It is pretty clear. Again, check out this article UpToDate
CC: “Chest pain”
HPI: 67 year old male from Bolivia presents to the Emergency Department with chest pain that is central, non-radiating, sharp, and lasts for only a few seconds. Chest pain has been present for years, however it has been acting up more lately. He has never gone to the doctor before today. Today his son felt that he should have his chest pain evaluated. He also endorses the occasional brief episode of palpitations. He denies pre-syncope, syncope, and diaphoresis. At his baseline he does become short of breath when he goes upstairs or walks more than a half kilometer. This shortness of breath has been present for years. He feels that he occasionally has fevers but he does not own a thermometer. He also has a long history of constipation for which he tries to drink plenty of fluids and eat foods that are high in fiber. He denies headache, abdominal pain, weakness, dysuria, melena, hematochezia, hematuria, bleeding disorders, hearing loss, emesis, and dysphagia. He immigrated to the United States to live with his son who works at the embassy. The patient speaks no English, but is able to communicate with you via the interpreter. He grew up in a small village in the cloud forest of Bolivia. He is a farmer.
ROS: Negative except as listed above in the HPI.
PMH: Has never gone to the doctor and is not sure.
Past Surgical History: None
Family History: Both his mother and father had diabetes and HTN
Social History: Denies smoking. Endorses drinking “canaso” a sugar cane based home made liquor occasionally during holidays. He later states that he does love to dance cumbia and when he dances he drinks. Denies ever snorting cocaine or other recreational drug use. However, he did chew coca leaves daily for the majority of his life until he moved to the US.
Vital signs: BP 120/86, HR 102, RR 17, Temp 38.0, Pulse Ox 96% on room air
General: Appears his stated age.
Eyes: PERRL, mild conjunctival pallor, EOMI
Neck: Supple, no cervical LAD, no stiffness
Cardiac: Regular rhythm and tachycardic. No MRG.
Respiratory: CTAB except for some faint bibasilar crackles.
GI: Abdomen is soft, non tender. No distention, rebound, guarding, or masses.
Musculoskeletal: Moves all extremities equally. Strength bilaterally 5/5 with regards to bicep flexion, tricep extension, hip flexion and extension, knee flexion and extension, dorsiflexion and plantar flexion.
Skin: Multiple large scars on his lower leg. He states that they are from machete accidents.
Neurological: Awake and moving all extremities spontaneously. No facial droop. Pupils are equal, round and reactive to light. Strength is 5/5 in upper and lower extremities bilaterally. No ataxia.
Extremities: +2 pitting edema.
#1. Which is associated with the most likely cause of the patient’s presentation.
A. Anopheles mosquito
B. Reduviid bug
C. Sandfly- L. donovani
D. Taenia Solium
#2. What other symptom/exam finding is most associated with this disease?
C. Painless skin ulcers
#3. What is the disposition for this patient based on the information presented above?
A. Admit to medicine with Infectious Disease Consult
B. Cardiac Catheterization
C. Discharge to home
D. Observation unit with telemetry
1 . B: This case is most consistent with a patient suffering from Chagas disease ( T. Cruzi). The triad of dysphagia, cardiomyopathy, and constipation are most commonly seen. The vector lives in the walls and roofs of houses in Central and South America. It can be eradicated completely with simple public health home remodeling. Chagas disease can be obtained from bug bites or via blood transfusion. Trypomastigotes migrate to the smooth muscle, cardiac muscle and autonomic ganglia of the heart, esophagus, and colon (1).
The problem transcends the borders of Bolivia. In Latin America 18 million people are infected and approximately 30% these individuals develop major heart disease decades after the acute infection. The WHO warns that 100 million people are at risk, and it is estimated that Chagas disease causes four times the burden of malaria, schistosomiasis, leprosy and leishmaniasis combined (2). Great strides have been made in eliminating the vector through public health strategies; however, many patients will continue to progress from the Intermediate Stage (seropositive but asymptomatic) to the chronic symptomatic phase (irreversible dilated cardiomyopathy, megacolon, and mega-esophagus). Thus a treatment for the larger number of patients with Intermediate Chagas disease is crucial.
Chagas disease includes patients with both asymptomatic and symptomatic disease. It is unclear on how we should go about treating these different subgroups of patients, especially those in the chronic phase.
The majority of experts agree that acute Chagas should be treated with Benznidazole (BZD). Acute infection is asymptomatic in most cases, but can present with malaise, fever, lymphadenopathy, mild splenomegaly, myocarditis and meningoencephalitis. If acute Chagas is detected, the patient should receive treatment. Up to 70% of these acute patients remain xenodiagnostically and serologically cured. No RCTs have been conducted on long term benefits of treating acute Chagas; however, it is generally accepted that all acute disease and reactivated disease should be treated with trypanocidal therapies (3).
Chagas can be diagnosed with the Chagas StatPak. The manufacturer reports a sensitivity of 98% and specificity of 95%. In order to officially have the diagnosis of Chagas a patient also needs to test positive with either the PCR or ELISA technique.
The two main trypanocidal medicines in use since the 1960s are Nifurtimox (NFTMX) and Benznidazole (BZD). Both of these medications are reported to have high noncompliance rates due to side effects, especially NFTMX. Side effects of NFTMX include nausea, vomiting, abdominal pain, weight loss, severe anorexia, paresthesias, insomnia and seizure. Side effects are seen in up to 40% of patients treated with NFTMX. The most serious side effects seen are leucopenia, peripheral neuropathy, and allergic dermopathy (4).
The Romana sign, painless unilateral swelling of the eye, which is often quoted in the literature is extremely rare. Many seasoned Bolivian physicians have never seen it.
Mega-esophagus is a known complication of Chagas disease. Dysphagia is one of the classic findings of Chagas disease. This is due to damage to the myenteric plexus of the colon.
Sgarbossa’s criteria states that ST segment elevation of 1 mm or more that is concordant to the QRS in any lead receives a score of 5 points. ST segment depression of at least 1 mm that is concordant in leads V1-V3 is worth 3 points. ST segment elevation of greater than 5 mm that is discordant values a score of 2. If a patient has a score of at least 3 there is a 90% specificity for myocardial infarction. However, the criteria are not very sensitive (5).
Case Presentation by Dr. Megan Dougherty, MD
CC: unable to obtain due to clinical condition
HPI: The patient is a 19 years old male presenting to the ED from county jail for altered mental status. The patient has been in county jail for 5 days. He has a known history of psychiatric disease for which he was possibly given valproic acid (records are unclear). Per the officer escorting the patient, the patient has eaten or drank anything in several days and was found moaning on the floor shaking prior to arrival and that is why he is at the hospital.
Unable to obtain due to clinical condition
Past Medical History: Psychiatric disease
Surgical history: Unknown
Allergies: None known
Medications: Possibly valproic acid administered at the jail, but no officer was able to verify if and or what medications were administered daily
Family history: Unable to be obtained
Social history: Currently in county jail. Unclear as to whether the patient smokes tobacco, uses alcohol or illicit drugs.
Vitals: Temperature: 39.2, blood pressure: 189/122, heart rate 154, respiratory rate 27, pulse oximetry 92% on room air
Appearance: in acute distress, shaking all four extremities and looking at everyone in the room, moaning
Mental status: making good eye contact, does not speak but continues to moan
Eyes: Pupils are equal and are 4 mm.
HENMT: head: normocephalic, atraumatic. Nose: no nasal discharge or epistaxis. Mouth: mucous membranes are dry and chapped. Throat: mildly erythematous, no tonsillar hypertrophy
Cardiovascular: tachycardic, regular rhythm. There is a good S1 and S2 without any murmurs. 2+ pulses are felt in all extremities. There is no lower extremity edema.
Respiratory: Clear to auscultation bilaterally. There are no wheezes or crackles. The patient is mildly tachypneic but there are no retractions. The patient is moaning.
Abdomen: soft, non tender to palpation. There is no guarding or rigidity
Musculoskeletal: moving all four extremities. There is no tenderness to palpation of any joint.
Neurological: The patient does not follow commands. He has no facial asymmetry. He continues to have rhythmic jerking. He continues to moan incoherently. Patellar and biceps DTRs are 3+ bilaterally. There is no clonus.
Skin: hot and dry. There is no abrasion or rash.
EKG was obtained. It showed sinus tachycardia. Labs were sent. A CT of the head and a chest x-ray were ordered. The patient was given 4 mg of Ativan for agitation. The patient was also given four liters of fluid. He was given 650 mg of acetaminophen rectally.
After you return to the module, you get a call from radiology to come to their lair to help interpret the head CT. This is what they show you.
1. Based on this imaging, what other imaging do you need?
A. soft tissue neck
B. CT neck
C. chest x-ray
D. CT thorax
2. What is the likely source of the subcutaneous emphysema?
C. necrotizing fasciitis
D. injection drug use
3. If imaging modalities chosen do not show source of subcutaneous emphysema, what is the next step?
A. place chest tube
B. consult neurosurgery
C. consult the ICU
D. consult ENT
While the etiology of this patient’s alteration was not elucidated by the workup performed, the subcutaneous emphysema was cause for alarm for further workup into potential causes that may not have provided a unifying diagnosis. Certainly, infection, ammonia, NMS, or serotonin syndrome, and others were all a consideration in this altered, febrile patient with a history of psychiatric disorder.
Subcutaneous emphysema was first described in 1850, as a complication of a patient with asthma. Subcutaneous emphysema and pneumomediastinum are both known complications of asthma. First descriptions were by Dr. Laennec (who is known as the father of the stethoscope and was the authority on heart and lung sounds in his time) and also by Dr. Hamman. Most common cause of subcutaneous emphysema in modern days is found to be a pneumothorax and/or a chest tube that has become clogged.
Clinical findings of subcutaneous emphysema include soft tissue swelling as well as crepitus to palpation of affected areas. The crunch felt on palpation is sometimes describes as “rice krispies”. This emphysema is typically painless. The subcutaneous emphysema can spread along the soft tissue planes and can extend up to the neck and head if the chest is the primary source. If severe, the subcutaneous emphysema can cause compression of the upper airway and can also cause jugular venous compression. This can lead to airway compromise and possibly cardiovascular compromise. The patients can develop dysphonia and dysphagia when the subcutaneous air dissects into the tissues of the neck. In the most severe cases, the subcutaneous emphysema can be a cause of dyspnea and they may require a tracheostomy. If pneumomediastinum is present, auscultation of heart sounds will reveal Hamman’s sign (or Hamman’s crunch), which is heard on auscultation with heart, sounds a crunching or crackle sound. Pneumomediastinum also typically presents with severe chest pain.
Dr. Hamman first identified the presence of pneumomediastinum in postpartum women; hence Hamman’s sign is heard when there is pneumomediastinum. The pneumomediastinum is likely related to the increased intrathoracic pressure generated when the women is in labor.
There are many case reports of subcutaneous emphysema and pneumomediastinum. Most commonly reported are causes associated with positive pressure ventilation and those following tooth extraction, especially in musicians. Causes of subcutaneous emphysema include but are not limited to: labor and delivery, SCUBA diving, excessive phonation, excessive blowing, positive pressure ventilation, Valsalva type maneuver, asthma, pneumonia, bronchiolitis, tooth extraction, digestive tract surgery IVDA, necrotizing fasciitis, trauma including GSWs and stabbings. When no source of subcutaneous emphysema is found, called spontaneous subcutaneous emphysema. Careful investigation is warranted first before declaring spontaneous subcutaneous emphysema. CT Thorax is helpful in identifying sources in airway or GI tract. If imaging modalities do not show a source, it would be reasonable to have ENT scope the patient to evaluate the airway for any defects.
Management of subcutaneous emphysema is primarily supportive. Treatment of causes such as pneumothorax is warranted. There are case studies of treatment of severe subcutaneous emphysema with bilateral infraclavicular incisions down to the subcutaneous tissue that helps to provide a tract for the air to drain. There are also case reports of placing a subcutaneous drain.
Chotirmall, SH, Morgan, RK. (2014) Subcutaneous emphysema, BMJ Case Reports. doi: 10.1136/bcr-2013-20112
Choo, M, Shin S, Kim J. (1998) A Case of Spontaneous Cervical and Mediastinal Emphysema. J. Korean Medical Society, 13: 223-6.
O’Reilly, P, Chen, HK, Wiseman, R. (2013) Management of extensive subcutaneous emphysema with a subcutaneous drain. Respiratory Case Reports, 1(2): 28-30.
Roquin, A. (2006). Rene Theophile Hyacinthe Laennec (1781-1826): The Man Behind the Stehoscope. Clinical Med